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Full text of "Archives of neurology and psychiatry from the Pathological Laboratory of the London County Asylums 2.1903"

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Director of the Laboratory and Pathologist to the London County Asylums ; 
Physician in charge of Out-Patients, Charing Cross Hospital 


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Tabes in Asylum and Hospital Practice. By F. W. Mott, M.D., F.R.S. 1 

Introduction . 1 ‘ .. .. .. 1 

Current Views of Relation of Tabes to General Paralysis in Standard 
Text-books .. .. ... ..' .. .. .. .. 4 

Etiology of Tabes and £abo-Paralysis .. .. .. .... 10 

Statistics Relating to Syphilitic Antecedents by various Authors, 

after Redlich .. .. 11 

Statistics of Syphilis in Sixty-two Cases of Tabes Dorsalis .. .. 12 

Statistics of Syphilis in Sixty-two Asylum Cases of Tabo-Paralysis 13 
Birth and Death-rate of Tabic and Tabo-Paralytic Patients .. 14 

Statistics Relating to General Paralysis in Women .. .. .. 15 

Conjugal Tabes and Paralysis .. .. . - .. .. .. 17 

Post-mortem Table Results in Reference to Syphilitic Residua in 
Tabes, compared with the Post-mortem Results in Tabo-Paralysis 

and General Paralysis.22 

Racial Syphilis in Uncivilised Countries in Relation to Tabes and 
General Paralysis.. .. .. .. .. .. .. .. 23 

Stress, Physical and Mental, Exposure, Injury, Hereditary Pre¬ 
disposition and Intemperance.25 

Mode of Onset of Tabes and Tabo-Paralysis .. .. .. .. 27 

Decades at which the Onset of Symptoms occurred .. .. 27 


Eye Symptoms of Tabes and Tabo-Paralysis.30 

Inequality, Irregularity and Size of Pupils .. .. .. .. 31 

Section II.—Sensory Disturbances .. .. .. .. .. 36 

Method of Examination.37 

Subjective Sensory Phenomena of Tabes and Tabo-Paralysis .. 42 

Parsesthesia. .. .. .. .. .. 45 

Objective Sensory Disturbances.45 

Visceral Disturbances . .. .. _ .. .. 53 

Affections of Cranial Nerves A .. .. .. .. .. 62 

Diseases of the Bones and Joints .. .. .. .. .. 64 

Motor Disturbances.70 

Cerebral Symptoms. 71 


Morbid Anatomy and Pathology .. .. .. .. .. .. 259 

Notes upon the Pathology of Tabes and Tabo-Paralysis .. .. 307 

Amentia. (Idiocy and Imbecility.) By A. F. Tredgold, L.R.C.P.Lond., 


The Histological Basis of Amentia and Dementia. By Joseph Shaw 

Bolton, B.Sc., M.D., B.S.Lond., M.R.C.P.424 

The Pathology and Morbid Histology of Juvenile General Paralysis 
By George A. Watson, M.B., C.M.Edin. 




The Coagulation-Temperature of Cell-Globulin, and its Bearing on 
Hyperpyrexia. By W. D. Halliburton, M.B., F.R.S., and F. \V. Mott, 

M.D., F.R.S. 

The Prevention of Dysentery in the London County Asylums. By 

F. W. Mott, M.D., F.R.S.”. 

The Range of Immediate Association and Memory in Normal and Patho 
logical Individuals. By W. G. Smith, M.A.Edin., Ph.D.Leipzig 
Pathological Changes in the Medulla Oblongata in Acute Diphtheritic 
Toxaemia. By Charles Bolton, B.Sc., M.D., M R.C.P. 

Systematic Examination of the Central and Peripheral Nervous System 
and Muscles in a Case of Acute Alcoholic Paralysis with Mental 
Symptoms. By Sydney J. Cole, M.A., M.D., B.Ch.Oxon. 

Note upon the Choline Test for Active Degeneration of the Nervous 
System. By F. W. Mott, M.D., F.R.S. 










Tabes in Asylum and Hospital Practice. Plates I., II., III., IV., V., 

VI., VII., VIII. Figs. 1-48 .. 47, 50, 51, 67, 69, 81, 102, 104, 105, 107, 

108, 109, 111, 112, 113, 114, 115, 125, 126, 130, 134, 135, 136, 138, 140, 146, 

147, 157, 158, 160, 162, 174, 175, 179, 180, 192, 206, 239, 265, 268, 271, 274, 

277, 278, 282, 285, 306, 310, 313 

Amentia (Idiocy and Imbecility). Plates I., II., III. Fig. 1 420, 421, 422, 


The Histological Basis of Amentia and Dementia. Plates I., II., III., 

IV., V., VI. Figs. 1-24 .. 557, 567, 568, 569, 571, 572, 573, 574, 575, 
581, 584, 586, 587, 589, 594, 595, 596, 601, 602, 606, 607, 609, 613, 614, 617, 

618, 619, 620, 620a, 6206 

The Pathology and Morbid Histology of Juvenile General Paralysis. 
Plates I., II. 725, 726 

The Prevention of Dysentery in the London County Asylums. Plates I., 

II., III. Charts I., II., III., IV., V. Plans I., II. 741, 742, 743, 744, 

745, 752, 755, 766 

Pathological Changes in the Medulla Oblongata in Acute-Diphtheritic 
Toxaemia. Plate I. Fig. 1 .. .. .. .. .. .. 812, 834 

Systematic Examination of the Central and Peripheral Nervous System 
and Muscles in a Case of Acute Alcoholic Paralysis with Mental 
Symptoms. Plates I., II. Fig. 5 . 848, 857 


The preface to the first volume of the Archives of the 
Laboratory of the London County Asylums was kindly 
written by Sir William J. Collins, M.D., then Chairman of 
the County Council, and promoter of the foundation of the 
Laboratory. In it he pointed out “ that various momenta 
have contributed to the recognition of the need of more 
determined, systematic and exhaustive research into the 
causes of insanity,” but it has since been found that it is 
also within the scope of the pathologist to advance the better 
treatment of the insane by preventing the acquirement 
of communicable diseases during their residence in an 
institution. In fact, an enquiry which I undertook with the 
aid of Dr. Durham into the prevention of dysentery in the 
London County Asylums and the issue of a Report thereon 
has been in great measure the cause of delay in the publication 
of this volume. It is satisfactory, however, to find that the 
recognition of this disease as infective, and the adoption of 
a number of recommendations which we made, have been 
the means of diminishing the death rate, at any rate, at 
Claybury, where it was prevalent in an endemic or epidemic 
form for years; and it is not too much to hope that if all 
our suggestions, and the additional precautions noted in the 
article entitled “ The Prevention of Dysentery in Asylums,” 
be carried out, that the disease will occur only in sporadic 
cases, and seldom become endemic, or attain an epidemic 
form. It is interesting to find that the Commissioners in 
Lunacy, in their last Report, June 27,1902, have adopted the 
term Dysentery instead of Colitis, and initiated “ a plan 
based on that adopted by Dr. Mott to ensure the registration 
and notification of cases of dysentery and diarrhoea in 
asylums amongst members of the staff as well as patients,” 
and that they now recognise the fact that it is a com¬ 
municable disease. 

viii. Preface 

The recently adopted system of notification of tuber¬ 
culosis which I have instituted should prove of great value 
in showing the prevalence of this disease among inmates of 
the different asylums, old and new; on clay soil, on gravel, 
and on chalk ; in different forms of insanity ; the relation of 
the disease to length of residence and acquirement in the 
asylum, or its presence on admission. The opportunities 
afforded of making autopsies, and thus verifying the clinical 
results, will help to settle the question, whether a larger 
proportion relatively of the inmates of the London County 
Asylums die from tuberculosis than those outside of cor¬ 
responding adult ages. 

It is undeniable that a further and more accurate know¬ 
ledge of the important subject of tuberculosis in relation to 
insanity and its treatment in large institutions is very 
essential, and it is hoped that this new system of notification 
which the Asylums Committee have adopted may become 
general in England. The difficulties of diagnosis of tuber¬ 
culosis in the insane are very great, as they do not expecto¬ 
rate, and often they resist physical examination either by not 
breathing, or by shouting and struggling; but the pathologist 
can obtain accurate statistics of the prevalence of the disease 
by careful and systematic post-mortem, examination. Thus, 
in a year or two, reliable evidence will be forthcoming to 
decide many of these points, and to help the authorities in 
determining the best course to adopt for its prevention. 

Another work which I have undertaken, and the import¬ 
ance of which is now widely recognised, is an investigation 
into the relation of syphilis to insanity. In the first volume 
of the Archives I showed that there was good ground for 
believing that the most important and possibly the essential 
cause of general paralysis, a disease which affects a large 
class often of the best and ablest minds of our town popula¬ 
tion, is syphilis, which is a communicable, therefore a 
preventible disease. In the present volume I show that 
etiologically general paralysis is identical with tabes dorsalis, 
therefore a large part of these and other organic nervous 
diseases affecting the community are due to syphilis. 

The same experience applies to ophthalmic practice. 

Preface ix- 

Blindness, paralysis, physical and mental incapacity, are too 
often, therefore, the result of a preventible disease. At the 
last annual meeting of the British Medical Association at 
Manchester, I opened an address in the Medico-Psycho¬ 
logical Section on the relation of syphilis to insanity. The 
subject was fully discussed with the result that a resolution 
was unanimously carried urging the authorities to take some 
steps to prevent the spread of syphilis. Too much reliance 
need not be placed upon unanimous expressions of opinion at 
meetings of this kind, for there are always a large number of 
people who, having no ideas of their own, are ready to follow 
the one which is at present uppermost; but on this occasion 
there were present a number of alienists holding some of the 
most responsible positions in the country, and who have had 
unexampled opportunities of examining the question and of 
forming an opinion based upon practical knowledge and 
experience. I feel convinced that such an unanimous ex¬ 
pression of opinion with regard to the relationship of syphilis 
to general paralysis could not have been obtained a few years 
ago; for many of those present have, after mature considera¬ 
tion, and I presume, investigation, changed their opinions, in 
support of the views which I uphold. The communications 
in this volume by myself, Dr. Watson and Dr. Bolton all 
emphasise this important relationship. Dr. Tredgold’s very 
interesting paper, which deals with 150 cases of idiocy and 
imbecility, shows that heredity is the most important cause 
of these conditions ; likewise, Dr. Bolton’s and Dr. Watson’s 
cases illustrate the important share heredity plays in mental 

My own cases, which deal only with one class of insanity, 
do not show the same preponderance of hereditary taint, 
and I am convinced that in dementia paralytica heredity is 
not such an important factor as in other forms of insanity. 

Dr. Tredgold also points out the importance of alcoholism 
and tuberculosis as etiological factors in the production of 
idiocy and imbecility. Syphilis, according to his observation, 
plays a less important role, but it is interesting to note that 
where congenital syphilis existed the juvenile form of general 
paralysis affected these imbeciles during adolescence. 



Of the influence of alcohol in the production of insanity 
and in the acceleration of all devitalising processes, there 
can be no question. The paper by Dr. Cole is upon a type 
of alcoholic paralysis and dementia which is frequently met 
with in asylums and hospitals. That by Dr. Chas. Bolton 
shows the influence of a specific poison in the production of 
an elective neuronic degeneration—such as the diphtheritic 
toxin and its effect upon the heart. Had space permitted, I 
should have published a number of other cases of alcoholic 
paralysis that I have investigated, but they must be held 
over for a future number of Archives by which time I hope 
that I may have had the opportunity of examining the 
brains and nervous systems of some acute cases of alcoholic 
poisoning uncomplicated by other toxic conditions, such as 

Since necessarily a year at least will elapse before the 
materials are complete for a third volume of “ Archives of the 
Laboratory.” I have been obliged to put two of the papers 
which have been awaiting publication into Brain, the 
Journal of the Neurological Society. Also much of my own 
completed research work has been held over, owing to lack of 

Anyone who will peruse the brief clinical notes of the 
large number of cases (selected from a much larger number), 
published in this volume, will find in the family histories 
a third cause of insanity, namely, mental worry and anxiety 
in its many forms ; and he would learn that it is seldom one 
factor alone that may be considered the cause of the patient’s 
affliction ; more often two or more conspire together. Stress, 
heredity, and often a poison in the blood are the factors 
I indicate ; and the problem of the prevention of insanity 
resolves itself into the prevention of syphilis, tuberculosis, 
and other communicable diseases—restriction of the abuse 
of alcohol, the removal of worry and mental anxiety—and 
the control of unsuitable marriages ; or at most the education 
of the public to the dangers, of the intermarriage of neuro¬ 
pathic individuals, or the marriage of an individual with an 
hereditary history of epilepsy or insanity with another of 
the neurotic temperament, in whom there is sometimes 
potential insanity. 



It might be asked, bow can we remedy mental stress and 
worry among the deserving poor ? I am of opinion that old- 
age pensions, or some such scheme for workpeople as exists 
in Germany and commencing to be put into practice in 
Sheffield and Birmingham, would do much to keep out a 
number of people from the asylums. Also the better 
housing of the poor and the reduction of rents, with cheap 
locomotion would, I am convinced, by removing the present 
terrible overcrowding, reduce a most fruitful cause of tuber¬ 
culosis, venereal disease, alcoholism, drunkenness, filth, and 

There is yet one point which it is desirable to mention as 
a result of both hospital and asylum experience, and that 
is the necessity of some earnest attempt being made to 
establish a means of intercepting for hospital treatment such 
cases of incipient and acute insanity as are not yet certifiable. 
It is probable that many would never come into the asylums, 
and a certain number of cases would thus come under ob¬ 
servation willingly, and in time to retard the progress of the 
disease. Practitioners could send doubtful cases for observa¬ 
tion and treatment to such hospitals, where, moreover, 
the opportunity would be afforded of improving their own 
knowledge as to the early signs of insanity. The import¬ 
ance of this idea, which I advocated in a report to the Council 
shortly after my appointment, is shown by the fact that 
it has been strongly taken up in Scotland by Sir John 
Sibbald and Prof. Clouston, who desire to see special wards 
established in connection with general hospitals. A mental 
case coming out of such a ward would not thereby be stig¬ 
matised as insane. 

Few, if any, of the hospitals in London have at present 
provision for these incipient and doubtful cases. 

If acute hospitals or receiving houses were established 
by the Asylums Committee, a number of cases which at 
present are taken to the asylums would never go there, and a 
better classification and a better knowledge of the physical 
and mental states of the patients transferred would ensue. 

The laborious researches of Dr. Joseph Bolton upon “ The 
Degeneration of Certain Layers of Cells of the Cerebral 

xii. Preface 

Cortex,” ai'e of great interest as regards the functions of the 
brain. They show that these particular cells which exist 
throughout the gray matter covering the cerebrum are deve¬ 
loped later than the other cellular structures ; that as the 
development of the mind takes place they increase in size 
and complexity, and consequently the strip of brain structure 
which they form increases in thickness; should, however, 
the brain possess an inherent defect of development such as 
occurs in idiocy and imbecility, these layers of cells, which 
are infinite in number, do not properly develop, and never 
attain the complexity of structure characteristic of the 
normal brain. Correspondingly, Dr. Bolton has shown that 
in proportion to the degeneration of these structures is the 
superficial destruction of the brain surface and the dementia, 
and this applies to all forms of insanity. There is therefore 
in this work a fundamental principle in the correlation of 
mind and matter. 

The careful histological examinations of the central ner¬ 
vous systems of eleven cases of juvenile general paralysis by 
Dr. Watson is a valuable contribution and addition to the 
article which I wrote on the subject in the first volume of 
the Archives, for a number of the cases reported there have 
since been thus systematically investigated. 

It is pleasant to me here to remark that Dr. Watson now 
holds the British Medical Association Scholarship; and it is 
to be regretted that the Board of Technical Education could 
not continue the Scholarship to Dr. Tredgold, whose scientific 
work gave such promise, and who has consequently with¬ 
drawn into general practice. Perhaps some other public 
body or private individual may be induced to come forward 
with the offer of a similar scholarship. 

A number of gentlemen have availed themselves of the 
opportunity of working in the Claybury Laboratory, and 
again, as Director, I wish to make known the fact that the 
Pathological Committee have always granted permission to 
applicants to make use of the splendid opportunities for 
obtaining material which this laboratory affords. Some 
medical men, however, have found the distance and difficulty 
of approach so great, as to debar them from the privilege. 

Preface xiii. 

Several have lived in the neighbourhood: for example, Dr. 
Gordon Wilson, of Chicago, Dr. Graham, and Dr. Smith, 
who has devoted a large part of his time to the experimental 
study of memory in the insane. His valuable contribution, 
which involved an immense amount of laborious observation 
and enquiry, is contained in this volume. 

It is a satisfaction to know that Dr. Smith’s work in 
experimental psychology has been recognised by his appoint¬ 
ment as lecturer at King’s College, London. 

With the permission of the Committee, I applied for 
recognition of the Laboratory by the London University. 
Unfortunately the Senate were unable to comply with this 
request, since the Laboratory is not situated in the area 
circumscribed by the new university. This appears to me 
a great pity, and the more so as the Board of Studies of 
Advanced Medicine, on which I have the honour to be one 
of the representatives of Pathology, has recommended that 
candidates for the M.D.London, can take pathology or 
mental diseases as a special subject. To those whose minds 
are bent upon neuro-pathology, what better opportunities 
could be obtained than by working in this London County 
Asylum Laboratory with the vast amount of material which 
could be placed at their disposal ? A number of the officers 
at the London County Asylums other than Claybury would 
take advantage of the Laboratory and its resources were it 
more central, and although it is of great advantage to have 
association of the Laboratory and the wards, still, a large 
proportion of cases will be observed to have been obtained 
from the other asylums. As I have the right of visiting all 
the asylums and of seeing the clinical aspects of the cases 
during life, I see no objection to having the Laboratory 
placed in London, where its field of usefulness would be 
greatly extended, and it might thus be made a centre of 
neuro-pathological science. 

Two gentlemen have already distinguished themselves by 
theses composed from work done in our Laboratory, and 
Dr. Pugh, who at my suggestion undertook a research upon 
“ The Alkalinity of the Blood in Epilepsy,” was fortunate 
enough to obtain a gold medal at the University of Edin- 

xiv. Preface 

burgh. This will appear in the next number of Brain. 
Dr. Cole’s thesis was successful in obtaining for him the 
M.D.Oxford, which University, however, confers no special 
distinction in addition to the degree. 

It has been of inestimable advantage to me to have 
had the co-operation of so distinguished a physiologist as 
Professor Halliburton, F.R.S., who has been my collaborator 
in one of the papers in this volume and in several papers 
on the “ Chemistry of Nerve Degeneration ” in the Philo¬ 
sophical Transactions of the Royal Society. Since he is 
Director of the Laboratory at King’s College which, unlike 
mine, is licensed for vivisection, he has performed all experi¬ 
ments incidental to the researches we have in recent years 
carried out. I find it necessary to publicly state this, and 
to repeat the fact that no experiments on living animals 
have ever been made or contemplated at the Pathological 
Laboratory of the L.C.A. 

The utility of pathological work cannot be gauged solely 
by the immediate results obtained, but every additional fact 
towards the elucidation of the complex structure or bio¬ 
chemical conditions of the nervous system in health and 
disease may be the starting point of some valuable discovery, 
and a new technique or method of observation may not only 
lead to work by its discoverer, but by a crowd of other 
workers who see in it future developments from other points 
of view. 

In conclusion, I will take the opportunity of thanking 
my former assistant, Dr. Hamilton Wright, for the histo¬ 
logical notes of several of the cases of tabo-paralysis, also to 
acknowledge my indebtedness to Messrs. John Murray and 
Co. for kindly allowing me the use of two blocks (figs. 25 
and 29), prepared from photographs which I supplied to 
Dr. Poore for his work on “ Forensic Medicine.” 

Frederick Walker Mott. 

25, Nottingham Place, W., 
December, 1902. 





BY F. W. MOTT, M.D., F.B.8. 


As I have pointed out in an article on “ Brain Syphilis,” 
an artificial classification of diseases obtains owing to our 
system of administration of relief to the suffering poor, by 
which asylum doctors see particularly those cases with 
mental symptoms, while hospital physicians meet with 
those cases especially which manifest physical signs of 
paralysis, sensory disturbances, &c. Thus it is with tabes 
and general paralysis. But in the almost unique position 
in England which I hold, of being able to study diseases 
both in hospital and asylum practice, and with the vast field 
which the latter offers to me as Pathologist to the London 
County Asylums, I am enabled to study all types of this 
disease from cases presenting purely spinal symptoms, to 
cases presenting mental symptoms which would lead to a 
diagnosis of general paralysis. 

In order to increase my field of observation, and also 
with the knowledge that some of the cases might event¬ 
ually come under further observation at one or other of 



the various asylums, I have visited a number of the infir¬ 
maries in order to study cases of tabes dorsalis in the 
paralytic stage or with premonitory mental symptoms. 
Some of these cases have since come into the asylums and 
died; others, I have found, had relatives, consanguineous or 
conjugal, dying in the asylums. I have been enabled to 
obtain thirty post-mortem examinations, and a systematic 
macroscopic and (in the great majority of instances) micro¬ 
scopic examination of the brain and spinal cord has been 
made of each ; frequently, also, the spinal ganglia, peripheral 
nerves, optic nerves, retinae, and other structures, have 
been examined. 

In some of these cases a full and detailed report will be 
given; but where it is only wearisome repetition, this will 
not be done; but the facts will, I trust, be accepted as true, 
being deductions from my personal observations on many 
thousands of sections of the central and peripheral nervous 
systems. Likewise with the clinical notes of the cases, 
which include more than sixty cases of tabes dorsalis and 
sixty cases of the tabetic form of general paralysis, I shall 
only record in full those cases which present some very 
interesting facts or rare condition. 

I have examined systematically the sensory disturbances 
in fifty cases of tabes dorsalis, and in a number of such 
cases of tabetic general paralysis which were capable of 
giving reliable answers ; also other clinical signs and symp¬ 
toms, including the mental condition. The amount of 
work involved in this can only be appreciated by those who 
have had a similar experience, and, of course, this research is 
not yet ended, for the majority of the cases I have observed 
clinically have not yet come to the post-mortem table. I 
found it advisable, owing to the vast amount of material 
at my disposal, to limit my observations to one class of 
disease, and in selecting this, tabes dorsalis, I thought it 
was possible to associate some of the mental disturbances 
with the changes which one meets in the nervous system, 
and to show that the illusions, delusions, and hallucinations 
have an organic basis, and that there is a great analogy 
between the paroxysms of pain, the visceral crises of tabes, 



and the epileptiform fits, attacks of mania, delirium, hallu¬ 
cinations, and other mental disturbances which occur in 
general paralysis. 

In the study of these cases, just as one can trace all 
grades of organic lesions from the purely spinal, through 
spinal with slight cerebral change, to extreme cerebral 
change and slight spinal change, so one can trace corre¬ 
sponding clinical symptoms. Many cases begin with marked 
spinal change and accompanying spinal symptoms ; there is 
then a sudden or gradual outburst of mental symptoms 
and the spinal sink into the background. So much may 
the cerebral symptoms overshadow, obscure, and even 
obliterate the spinal symptoms, that they may be overlooked 
and disregarded. In fact, I have seen so many cases in 
which ataxy has disappeared with the progressive cerebral 
disease that I am reminded of the truth of the dictum of 
Hughlings Jackson that “ one half of the symptoms of 
nervous diseases are due to the unbalanced action of healthy 
structures.” That many of these cases were in the second 
stage of tabes, and yet evinced after the onset of the mental 
symptoms little or no ataxy in their movements, was shown 
by the examination of their spinal cords and posterior roots. 
At a discussion opened by myself at the Pathological 
Society upon the unity of tabes and general paralysis, most 
of the leading authorities—Sir William Gowers, Dr. 
Buzzard, Dr. Savage, Dr. Ferrier, Dr. Hale White, Dr. 
Head, and others, who spoke—were of the opinion that 
etiologically and pathogenetically the two diseases were 
identical. This view has not, however, found its way into 
the text-books, although, as a matter of expediency, it is 
often adopted by physicians, for when a noble or distin¬ 
guished patient suffers from grandiose delusions and other 
signs of the progressive brain disease which in a few years 
will terminate fatally, it is given out that he is suffering 
from locomotor ataxy. I maintain that etiologically and 
pathogenetically there is one tabes which may begin in 
the brain (especially in certain regions), or in the spinal 
cord in certain regions, or in the peripheral nervous struc¬ 
tures connected with vision, or in nervous structures con- 



nected with the viscera, constituting, therefore, different 
types, any of which may be present or be associated with 
one or all of the others. More and more we are coming to 
the opinion that syphilis is the cause of the degenerative 
process evinced, and although many authorities will not go 
so far as Mobius, who considers that all cases are meta¬ 
syphilitic, or Fournier, who calls them para-syphilitic, still 
the majority of neurologists and alienists in England and 
Germany believe that syphilis is the main causal factor of 
this polymorphic disease. The experimental observations 
of Krafft-Ebing, and the fact that practically all cases of 
hereditary tabes and almost all cases of juvenile general 
paralysis can be proved to have occurred in the children of 
syphilitic parents strongly supports the syphilitic doctrine 
of this disease. 

Current Views op Relation of Tabes to General 
Paralysis in Standard Text-Books. 

Since Westphal showed the existence of posterior- 
column-sclerosis in cases of general paralysis, nearly all 
neurologists have gradually come to recognise a close alli¬ 
ance between tabes dorsalis and general paralysis. It would 
be impossible to relate all the literature that has been 
written on this subject, but I will give a few quotations 
from some leading alienists and neurologists. The first in 
this country to recognise the association was Dr. Savage, 
and he says (Article on Locomotor Ataxy, “ Tuke’s Dic¬ 
tionary of Psychological Medicine”): 

“ Locomotor ataxy and insanity may occur in the same person 
and be unconnected, or locomotor ataxy may precede the develop¬ 
ment of associated mental symptoms, or locomotor ataxy symptoms 
may be the first indication of general paralysis of the insane. 
Locomotor ataxy and general paralysis may to some extent 
alternate, so that while the ataxic symptoms are fully developed 
the mind is clear; and while the mind is disordered the ataxy 
becomes less or is absent. Locomotor ataxy may have the 
following special reactions mentally: there may be during the 
course of the disease mental crises; a patient who is recognised 
as suffering from locomotor ataxy suddenly becomes manaical. 



In these cases generally there is more or less suspicion, or a 
tendency to retaliate on those who are supposed to be causing the 
painful sensations in various parts of the body. These maniacal 
attacks are of short duration, but may recur at regular intervals. 
There may be insane interpretations of the ordinary crises, so that 
one patient says that his bowels have been twisted by his perse¬ 
cutors, and another says that red-hot irons have been thrust in 
his feet and eyes, and another complains that unnatural means 
have been used to withdraw his semen. The ordinary symptoms 
of locomotor ataxy are insanely explained in other ways. The 
mental symptoms of these cases may be acute or chronic; in the 
former case they may alternate, so while the delusions exist the 
ataxy is better, and vice versd; or the insanity may be transient 
or recurrent. In some cases the insanity may be as chronic as 
the locomotor ataxy, but there seems to be little tendency to 
dementia in these patients. The most common relationship of 
insanity and locomotor ataxy is met with in general paralysis of 
the insane, and in this the symptoms of both may begin at the 
same time, so that with extravagance, boastfulness, and lust 
ataxic weakness may develop. In other cases locomotor ataxy is 
the first symptom, and after a period varying from one to seven 
years, other symptoms point to the existence of general paralysis. 
In some cases the general paralysis has first been recognised, and 
it is only later that locomotor ataxy is recognised.” 

Mickle (Article on General Paralysis : Tuke’s Dictionary of 
Psychological Medicine ”) merely states that “ the ascending form 
of general paralysis must be distinguished from tabes dorsalis, at 
times a difficult task,” otherwise hardly any notice is taken of 
this form of general paralysis. 

Bevan Lewis (“A Text-Book of Mental Diseases ; Pathological 
Anatomy of General Paralysis,” p. 566). Referring to spinal 
symptoms, this author groups cases into four arbitrary divisions. 
I will content myself with quoting in full his remarks in regard to 
the second group, comprising from the very onset notable tabetic 
symptoms :—“ The cerebral symptoms are often so greatly in 
abeyance as to arouse the doubt whether we are not here engaged 
with a genuine tabes dorsalis of spinal origin. The disturbance 
of sensation, the abolition of the deep reflexes, the ataxic gait, are 
all so prominent that we are apt to attribute such symptoms to a 
primary implication of the cord itself. (This, I am sure, is the 
actual cause of the symptoms, and my own observations show 
that we should be right in thus accounting for them. F. W. M.) 
Yet in this tabetic form of general paralysis we must usually 
witness complete subsidence of the special spinal symptoms, the 



tabetic gait passes off, the knee-jerk returns, and then the full 
development of the cerebral symptom is established, or what is 
not infrequent, the sensory implication of the cord becomes a 
motory affection, and the spastic paraplegia replaces the anaesthesia 
and ataxia. (My observation is that these clinical facts are right, 
and the inference wrong. F. W. M.) There has been a tendency 
to regard the later evolved cerebral derangements of typical 
general paralysis established in a well-marked tabetic case as due 
to an ascending change—that is, propagation by direct continuity 
of diseased tissue, thus making a system disease of the spinal 
cord the originating factor of the subsequent ‘ lesions of general 
paralysis.* ** Dr. Lewis would look for the explanation rather 
through the vaso-motor agency operating on nervous systems in 
physiological sympathy with their higher centres. I will discuss 
this point later, but with the first statement, that it is not an 
ascending change, I quite agree. 

On page 319 Dr. Lewis states-: “ In tabetic forms of general 
paralysis the oculo-motor anomalies almost invariably precede the 
tabetic signs of abolished knee-jerk, and the pupils failing to dilate 
on shading or cutaneous stimulation, a paralytic myosis (moderate) 
eventually passes into a genuine spastic myosis from the 
irritation of a diseased process advancing upon the constrictor 
nucleus.* * 

On page 322: “ We may enumerate the association of a paretic 
or tabetic gait with the abolition of the deep reflexes and like 
irido-motor troubles. The tabetic gait occasionally associated 
with this absence of the knee-jerk is occasionally peculiarly 
disorderly, hurried, spasmodic, and insecure.** 

Regie ('‘Manuel Pratique de Medicine Mentale **) says: 
“ Since attention has been drawn to the mental state of tabetics, 
psychic troubles have been recognised more frequently in them; 
they are generally disturbances of intelligence and modifications 
of character which are revealed by irritability, bad temper, 
moroseness, hypochondriasis, depression and suicidal tendencies; 
at other times this may happen in the pre-ataxic stage; sensory 
troubles may be manifested, consisting of illusions, or more or less 
conscious hallucinations, principally affecting vision, hearing, or 
general sensibility; but the psychic disorders may not terminate 
here, and in certain cases insanity may co-exist. Pierret et 
Rougier, who have made a practical study of this insanity, have 
shown that more often it was a state of melancholia, with vague 
ideas of persecution and confused hallucinations. (A number of 
cases of this kind in my experience will be given later on. 
F. W. M.) The patients accused persons of wishing to poison 



them, of making them burn; they complain of hearing that 
injuries will be done to them, of experiencing a bad taste in their 
food and in their mouth, of experiencing electricity in their limbs 
and disagreeable sensations; the delirium may present itself in 
the hypochondriacal form or in the ambitious form, as in general 
paralysis. Finally, tabes may be accompanied by enfeeblement 
of intellect, which may present great difficulties in distinguishing 
it from general paralysis. In some cases the disease assumes a 
hybrid form, and seems to be both tabes and general paralysis. 
The latter may be primary or consecutive to locomotor ataxy. 
When it begins thus by spinal phenomena it is given the name of 
ascending general paralysis. (This, I hold, is wrong. F. W. M.) 
This is the place to repeat that general paralysis and tabes are 
diseases absolutely similar as regards origin and nature, and that 
they have the closest relation to one another. It is not rare to 
see general paralysis begin or end by symptoms of ataxy, and in 
certain cases present during the course of the disease a mixture 
of spinal and cerebral symptoms.” 

Krafft-Ebing (“ Progressive allgemeine Paralysie, Nothnagel’s 
System ”), one of the most energetic supporters of the syphilitic 
doctrine of general paralysis, strangely enough does not devote 
much attention to the relation of this disease to tabes dorsalis. 
Oja page 11 he refers, under motor disturbances, to tabetic 
symptoms in the form of temporary ocular paralyses, myosis and 
reflex pupil rigidity in the prodromal stage. On page 21 the 
disease of the spinal cord appears as “atrophy of nerve-fibres 
with consecutive development of connective tissue, and it may be 
looked upon as corresponding with the tabetic process. It is most 
strongly developed in Goll’s column, and in the cervical cord is 
mostly limited to this tract. (Westphal.)” 

On page 49 : “ The motor defects of the trunk and extremities 
are different in nature, and partly due to muscle insufficiency, 
partly ataxy, partly tremor. They arise in part from cortical 
changes, partly from pre-existing and complicating changes in 
spinal tracts. The gait may be paralytic, spastic, or ataxic.” 

On page 54 : “ In about 4 per cent, of the cases of paralysis, 
one finds tabic optic atrophy.” 

Page 73 : “ Often spinal cord changes, such as diseases of the 
posterior columns arising from the same predisposing cause— 
syphilis, whereby simultaneously or successively spinal cord or 
brain are affected. The tabetic process may come on with the 
paralytic or precede it.” (He does not, however, mention it in 
the differential diagnosis. F. W. M.) 



Sir William Gowers (‘‘Diseases of the Nervous System,*' 
Spinal Cord, p. 466) says : 

“ Another very important and frequent complication of tabes 
is general paralysis of the insane. The two diseases have many 
alliances; it is probable that syphilis is the chief cause of 
general paralysis as well as of tabes. Keflex irido-plegia is 
common in both diseases; the two maladies are often combined, 
and the symptoms of one or the other may preponderate. Thus 
many general paralytics present symptoms of tabes, and its 
characteristic lesion is found after death. On the other hand 
cases of tabes may present slight symptoms of general paralysis, 
perhaps only slight optimism and mental weakness, which may 
remain subordinate or may increase to a pronounced or prepon¬ 
derate degree; it may be difficult to say in which category a case 
should be placed. It is sometimes said that a disease may 
commence as ataxy and change to general paralysis, but a more 
correct expression of the facts is a co-existence of the two affec¬ 
tions and the dominance of the symptoms of one or the other/* 

Clouston (“ Mental Diseases,” 5th Edition, 1898, p. 390) 

“ The most marked variety of general paralysis is the 
peripheral form, where the pathological process does not begin in 
the cortex of the brain but in the cord (the tabic form), or in the 
neuronic portions of the organ of special sense (the sensory form), 
or in a peripheral nerve (the peripheral form) spreading upwards 
by pathological propagation along the connecting nerves in the 
lines of physiological function till it reaches the brain cortex. 
These varieties are rare, but distinct enough when they occur, 
and very interesting. They would seem to imply that the patho¬ 
logical process of general paralysis resembles the progressive 
Wallerian degeneration.** 

This assumption of Prof. Clouston is purely hypothetical; I 
have never seen degeneration of the fillet in the twenty-five cases 
of the tabic form of general paralysis which I have examined 
microscopically. If there were a progressive degeneration spread¬ 
ing up to the cortex along the path taken by the kinsesthetic 
impulses, there would be a continuation of the degeneration of the 
column of Goll, which was invariably present in all these cases, 
through the posterior column nucleus, the internal arciform fibres 
and the fillet; but this I have never seen. Neither have I seen 
any evidence in support of a process spreading up from the peri¬ 
pheral nerves ; no doubt. Dr. Clouston has put in a hypothetical 
way the so-called ascending form of general paralysis. This author 
refers to six cases of the typical tabic form which he has seen; 



strangely enough in an otherwise admirable text-book he almost 
disregards the influence of syphilis as a causative factor in the 
production of general paralysis. He refers to the opinion of Dr. 
Drummond, of Newcastle, but surely the work of Fournier, and a 
large number of other Continental authors who have worked at 
this subject should not have been disregarded ; and whatever Dr. 
Clouston’s own opinion on this subject may be, in a text-book the 
other side of the question should have been stated, seeing that it 
is a prevailing opinion in England, America, and on the Continent, 
that, if syphilis be not the sole factor, it is the most important 

Mobius (“ Ueber die Tabes,” Berlin, 1897), in one of the most 
valuable monographs that has appeared on the subject, on page 6 
of the introduction, points out that Tiirck, Baillarger, Simon, 
Westphal, Falret, Magnan, and others have studied both the 
clinical as well as the anatomical relations of the two diseases. 
However, it is only recently that the opinion has been advanced 
that really both diseases are of the same sort; that we call it 
tabes when especially the centripetal nerve-fibres are diseased, 
and general paralysis when especially the cerebral cortex is 

“ This view is by no means accepted by all, still I maintain it 
is correct. Both diseases have the same cause, for both are 
meta-syphilis ; in both there occurs a primary atrophy of nervous 
structures. Important symptoms, especially reflex pupil-rigidity 
and ocular muscular paralysis, are in both nearly equally fre¬ 
quent ; in many tabetic cases, slight changes appear to be present 
in the cerebral cortex, which essentially resemble those of general 
paralysis. Still more frequently are spinal changes, loss of knee- 
jerks, disease of the posterior columns present in paralytic 
patients. The tabetic cases come under the neurologists, and the 
paralytic cases under the alienists.” 

On page 31 on “ The Brain Symptoms of Tabes,” Mobius 
says :—“ Attacks of migraine, epileptic attacks, apoplectiform 
attacks, and psychical disturbances may occur; it is, however, 
more correct to consider these complications as symptoms of 
progressive paralysis in tabetic patients. They represent an in¬ 
complete paralytic disease of the cerebral cortex, and they corre¬ 
spond to the transitions between the cases with isolated paralytic 
symptoms and those with undoubted progressive paralysis.” 

Marie (“ Lectures on the Spinal Cord,” Sydenham Society 
Trans., p. 292) says: 

41 The psychical derangements which occur in the course of 
tabes are not infrequent, but vary considerably; and Dieulafoy 



was able to apply the term 1 Tabid Insanity ’ to the condition 
which existed in some patients, while others present similar 
symptoms which are but slightly pronounced, and may be either 
transitory or permanent, or possibly occur in paroxysms (Fournier). 
He distinguishes the moral from the intellectual derangements— 
the former he attributes more especially to the weak condition of 
the patient, and he remarks that notwithstanding the agonising 
pains the patients frequently feel, they are rarely found to commit 
suicide; while, on the other hand, in certain affections, notably 
those of the bladder, suicide is relatively more common. This is 
an interesting point in connection with the psychology of the 
tabic patient. (Both these symptoms are among the most 
frequent in tabes, and I have recollections of several patients who 
have attempted suicide on account of the pains and the miserable 
depression occasioned by an incurable disease, and accordingly 
been admitted to the asylum. F. W. M.) As regards the 
intellectual disorders, they are far less frequent, and if truly 
pronounced, depend upon the association of cerebral lesions with 
those of the spinal cord. Tabes is in that case most often found 
to be complicated by general paralysis of the insane. Such cases 
are rare, if not exceptional.” 

Etiology of Tabes and Tabo-Paralysis. 

In the first volume of the Archives I gave a pretty full 
account of the literature in reference to the relation of 
syphilis and general paralysis both in the adult and juvenile 
form ; since then, the percentage of syphilitic antecedents in 
general paralysis has attracted more attention in most of the 
London County Asylums, and I notice in the report of 1901 
from Bexley Asylum that Dr. Stansfield gives 80 per cent, of 
the general paralytics with signs or history of syphilis. Dr. 
Thomas, of Hanwell, informs me that amongst the male 
admissions at Hanwell during the past eighteen months, 
80 per cent, gave a syphilitic history. Dr. Bolton’s statistics 
give similar results. 

In 1863 Eisenmann and Topinard both expressed the 
opinion that syphilis was probably the cause of tabes ; 
Westphal (1881), on the other hand, not only said that it was 
not proved, but it was not probable that syphilis was the 
cause of tabes. It was not until Fournier in 1876 brought 


forward a series of thirty cases of tabes in which syphilitic 
antecedents were proved in twenty-four, that really attention 
was directed to the subject. As in general paralysis, so in 
tabes it was received with scepticism by the majority of the 
profession. Yulpian supported Fournier, and the latter 
collected more cases and in 1882 brought forward 103 cases 
of tabes, ninety-nine of which had suffered with syphilis, 
that is, over 90 per cent. Later he increased the numbers 
to 146, or 93 per cent. Erb in Germany, and Sir William 
Gowers in England collected cases, but it is especially the 
work of the former that has substantiated the doctrine of 
Fournier. Erb commenced collecting cases in 1879 and in 
the year 1897 his cases amounted to 900 of which 90 per 
cent, had suffered with syphilis. He found in 6,000 other 
nervous cases on the same basis only 20 per cent. 

Westphal, Charcot and Virchow were always opponents 
of the doctrine, but the greatest opponent has been Leyden. 
Various authors have given different results. Very much 
depends on what each considers sufficient evidence to warrant 
the assumption of syphilitic antecedents. In a certain 
number of cases there is a history, of a soft sore ; in a large 
number it would be perfectly legitimate to consider this was 
syphilis, even if the secondary symptoms were so mild as not 
to have been noticed by the patient. In women, still-births 
and miscarriages or sterility would indicate probable, but 
not certain, syphilis. 

Statistics Relating to Syphilitic Antecedents by 
Various Authors, after Redlich. 


.. 45 per cent. 


.. 50-7 „ 


. 51 „ 


..60 „ 


..60 „ 


• 60 „ 


•61 „ 


.. 63-5 „ 

Gowers .. 

•70 „ 

Mendel .. 

•70 „ 


•70 „ 


.. 72 per cent. 


75 „ 


75 „ 


• 76 „ 


.. 85 


..90 „ 


..90 „ 


•90 „ 




..100 „ 



There is a very considerable difference in the statistics of 
men and women as regards syphilis. Erb’s statistics (1896) 
are in women 57 per cent, certain syphilis, and 30 per cent, 
highly probable. Minor published eight cases of tabes in 
women in all of whom syphilis was present. Redlich’s are 
23 - 4 per cent. 

Max Nonne points out that as interest in this question 
was increased the authorities who had previously only found 
a small percentage of tabetic patients suffering with syphilis 
were led, as the enquiry progressed, to increase their per¬ 
centages ; thus Berger’s statistics rose from 20 to 43 per cent., 
those of Bernhardt from 21 to 60 per cent., Oppenheim’s 
from 17 to about 80 per cent., and Rumpf’s66 to 80 per cent. 
Minor’s observations relating to tabes are also of great 
interest. He showed that among4,700 non-Jewish Russians 
2'9 per cent, were tabetics, on the other hand among 698 
Jewish patients suffering with nervous diseases only 0.8 per 
cent, were tabetics. Functional nervous diseases are 
extremely common amongst the Jews, and yet tabes is com¬ 
paratively rare. This may be explained by the fact that the 
Jews are much less liable, to become infected with syphilis. 
Minor later showed that both tabes dorsalis and syphilis are 
five times as common among the non-Jewish Russians as in 
the Jews of Russia. (Among my cases there were three 
tabetic Jews. Two certainly had had syphilis and one 
probably. There were also three tabic paralytic Jews all of 
whom had signs and history of syphilis.) 

Statistics of Syphilis in Sixty-two Cases of Tabes 


In my own statistics there were forty-seven males and 
fifteen females. Of the forty-seven males, thirty-three (over 
70 per cent.) had certainly syphilis, fourteen were doubtful, 
three owned to gonorrhoea and two to soft sore ; nine denied 
infection, but only one of these was able to say that he had 
not been in the way of getting it, and this man very 
possibly may have been the subject of inherited syphilis or 
have acquired it in some unusual way when young (vide 


Case 1). In connection with this point I may mention 
that I had a patient not long ago under my care suffering 
with epileptic fits which were cured by mercury and iodide. 
The patient was aged 20 and I was informed that he had 
contracted syphilis when a little boy by being allowed to 
sleep with a shop assistant who suffered with the disease. 
Again, children may present no signs of syphilis on the body, 
and yet when a careful history is obtained, congenital syphilis 
can be proved to be the cause of a primary optic atrophy 
{vide Case 74), juvenile general paralysis, or tabes. 

Again, as an example of syphilis acquired in an unusual 
manner, I will cite a series of ten women infected in child¬ 
hood by a midwife {Lancet, p. 402,1895). Also, a number of 
glass blowers at St. Helens suffered with chancre of the lip. 
Many people are infected and never know they have suffered 
with the disease; but a larger number know and will not 
own up. 

Statistics of Syphilis in Sixty-two Asylum Cases of 

T abo-Paral ysis . 

Of fifty-four male tabo-paralytics and insane tabetics, 
forty-six of which were personally seen and examined by 
me, there was a reliable history, or signs on the body, of 
syphilis in at least 75 per cent. In four cases there were no 
notes obtainable, and I did not see the cases during life. 
In four there were doubtful signs or history. In only one 
case was there no history of syphilis, no signs on the body, 
and a healthy family, but as everyone knows, this does not 
absolutely exclude a syphilitic infection. In the remainder 
syphilis was probable, or could not be excluded. 

There were eight women. In only two were there 
definite signs on the body ; the history, however, of 
the remaining six made it almost certain that they had 
been infected. One was probably a “ puella publica ” 
without friends. Another was a kept woman who had 
previously suffered with venereal disease, and had had 
several miscarriages. The remaining four had husbands 
who suffered with tabes or general paralysis themselves 
{vide pp. 18, 19). 



Birth and Death Rate of Tabic and Tabo-Paralytic 


Twenty-six tabetic men were married, and had eighty-six 
living children, forty-seven dead, twelve born dead, and 
twenty premature births. Several were infected after 
marriage, and then followed miscarriages and dead children. 
It will be of interest to contrast the death rate of the 
children of ataxic patients of the two sexes. 

Amongst the fifteen females, fourteen were married 
women. Four of these were sterile, and had no premature 
births; all gave a definite history or signs of syphilis on the 
body. Of the others one had a living child after ten years 
of married life; she did not know that she had had any 
miscarriages, and there were no signs of syphilis on the 
body. Of the remaining nine, three had certain signs and 
history of syphilis, but all the nine had miscarriages, still¬ 
born and dead children. One woman was unmarried, and 
there was no history or sign of syphilis. The record of 
the fourteen married women as regards children was as 
follows: Four had no children and no miscarriages; ten 
had amongst them (each contributing, so that every one 
was capable of conception and of child-bearing) six living 
children, sixteen miscarriages, fourteen bom dead, and four 
dead in infancy. 

The eight females had amongst them sixteen mis¬ 
carriages or premature births, eight children dying in 
infancy, and ten children living, but the eight children 
dying in infancy, and five of the living children were 
contributed by one woman. 

The married male tabo-paralytics were thirty in number, 
and had sixty-eight children alive, twenty-six children dead, 
and twenty-seven miscarriages or bom dead. If we contrast 
these statistics of tabo-paralytics with the tabetic cases we 
find that they have fewer healthy and dead children. This 
is because they do not live so long after infection as the 
tabetics, moreover after removal to an asylum no further 
conception takes place, otherwise there is the same close 
similarity between the hospital and asylum cases. Adding 
the fifty-four males married, suffering with tabes or tabo* 



paralysis together, and contrasting them with the twenty- 
two married females, we find a remarkable contrast, showing 
that when the female is infected, the chance of living 
children being born is greatly reduced; correspondingly, 
there is an increase of dead children and miscarriages. 

; alive. 

Born alive, but 
died in infancy, 
or afterwards. 





Twenty-two married females, suffering 
with tabes or tabo-paralysis. Seven 
of these were sterile. 

Fifty-four married males, suffering with 
tabes or tabo-paralysis. 






| 76 



Several male cases were of interest because of a definite 
history of infection occurring after marriage : in these cases, 
miscarriages and abortions followed healthy children. It 
will be seen that very nearly 30 per cent, of the married 
women were sterile. Mendel 1 found that in 252 married 
female tabetics 32 9 per cent, were childless. 

Statistics Relating to General Paralysis in Women. 

By kind permission of Dr. Stansfield I am enabled to 
publish the following data from statistics furnished by Dr. 
Hubert Bond:— 

1 E. Mendel. “ Die Tabes beim Weiblichen Geschlecht,” Neurol . Central - 
blatt , 1901. 

The text-books teach that tabes occurs much more frequently in men 
than women : e.g. those of Obersteiner and Redlich, v. Leyden and Gold- 
scheider, Gowers, Oppenheim, Grasset. Erb gives 19*5 : 1, Fournier 26: 1, 
Kowshewnikoff 11: 1, Moczutkowsky, quite recently 15 : 1. 

Mendel’s statistics at his Polyclinic in Berlin:—Number of patients 
20,539 males, 21,825 females; total 42,464. Of these there were 725 male 
tabetics, that is 3*53 per cent., and 288 female tabetics, that is 1*31 per cent. 
There was, therefore, one tabetic woman to 2*7 tabetic men. 

He comes to the following conclusion. One can therefore say that the 
frequency of tabes in the female sex is essentially the same as progressive 
paralysis among the poorer classes, where about one paralytic woman to every 
three men occurs ; whilst in the well-to-do the relationship is improved five 
to ten. Tabes occurs at a somewhat later age on an average in women than 
men, the greatest frequency being from 40 to 45 years. Of the 288 cases, 
252 were married women, and thirty-five unmarried. Of the 252 married 
women, eighty-three were childless, 32 9 per cent. Kron found among 
thirty-three married tabetics ten sterile, 30 per cent. According to Gutt- 
stadt’s figures which agree with those of Mendel, 10 per cent, to 15 per cent, 
of sterile marriages occur among the same classes of non-tabetic married 



Of seventy female general paralytic cases there were fifty-two 
married women ; six cohabited with men ; four were juvenile 
general paralytic cases ; one was imbecile; seven were single 

Dr. Bond obtained the very high percentage of 34 out of 
70 with certain history or signs pointing to syphilis, and ten 
doubtful history. 

The following data were obtained from statistics kindly 
furnished me by Dr. Bailey, of Han well, relating to 118. 
female general paralytic cases 

Of 118 female general paralytics there were 102 married 
women ; two juvenile general paralytic cases ; three certainly 
had cohabited; eleven single, (?) virgins. 

The 105 women had 129 children alive, 117 children born 
alive but dead = 2-3 per cent. 

Of these women 34-5 per cent, were sterile, which is almost 
identical with Mendel’s statistics regarding tabetic women. 

Dr. Bailey’s statistics do not show more than 20 per cent, 
with a history or signs of syphilis on the body. 

This sterility may be explained by the fact that conception 
had not taken place, or that the embryo had died in the first 
month or so after conception. 

Statistics of Spencer Wells, Simpson and Sims, as well 
as of Guttstadt, show that married women are childless in 
10 to 15 per cent. In female tabetics and paralytics sterility 
is nearly three times as frequent as the average. In England 
the average number of children bom alive for each married 
woman is 4’5. It will be found that this corresponds nearly 
with the male tabetics and tabo-paralytics; but with the 
females suffering with this disease it is less than one for 

That we cannot prove more than between 70 to 80 per 
cent, of tabic and paralytic patients to have suffered with 
syphilis is no argument against the doctrine that both 
paralysis and tabes are post-syphilitic affections. Dr. Crocker 
has shown that in not more than 80 per cent, of true specific 
skin diseases can a history of syphilis be obtained. In sixty 
cases of syphilitic brain disease I could not obtain a history 
in more than 70 to 80 per cent. The very important experi- 


ence of Jadassohn and Hirschl, that only in one-half of the 
cases of undoubted severe syphilis is it possible to prove 
primary infection, and the statement of Lang that in one- 
third of the cases of tertiary syphilis the primary infection 
was not demonstrable, are arguments against those who will 
not be convinced that syphilis is the essential cause of tabes 
and general paralysis unless it can be proved in every case. 

Conjugal Tabes and Paralysis. 

Mendel, a supporter of the view that syphilis is the most 
important cause, of tabes and paralysis, published in the 
Neurologiaches Centralblatt (1888) five cases of paralysis and 
tabes occurring in married cotiples; and Dr. Baeeke, in the 
Monatschrift fur Psychiatrie und Neurologie, vol. 6, pub¬ 
lished seven of his own cases, and he gives a table with 
complete literature of sixty-nine cases. 

In 38 cases, syphilis certain. 

„ 11 ,, ,, probable. 

„ 2 „ „ denied. 

„ 18 „ „ unknown faets, but probable syphilis. 

Paralysis in both husband and Wife occurred in 27 oases. 
Tabes ,, ,, ,, ,, 22 ,, 

Paralysis in man and Tabes in wife ,, 14 ,, 

,, wife ,, „ husband „ 6 ,, 

■34 per cent. Tabes 
■ m one or other of 
the couple. 


This result agrees with Mendel’s statement that “ if each 
of the couple suffer with tabes or paralysis, the man is more 
frequently affected with paralysis.” The author also shows 
that the man as a rule suffers before the woman; the 
reason is obvious—the man- is affected with syphilis first, 
and is therefore more likely, but not certain to develop 
the syphilitic degenerative affection. Out of twelve cases of 
tabes in husband and wife the man was affected first in 

Dr. Moenkemoller (“Ueiber Conjugate Paralyse beziiglich 
Tabes,” Monatschrift f. Psych, u. Neurol., 1900, Bd. viii.) 




found that in 741 paralytics admitted to Herzberge Asylum 
during six years, there were seventeen cases of conjugal 
paralysis or tabes. Of these seventeen cases, in fourteen 
both husband and wife were affected with paralysis; in seven 
of these, however, one or other suffered with tabo-paralysis ; 
and in two the husband suffered with tabes and the wife 
with paralysis; in one the husband suffered with paralysis 
and the wife with tabes. The husband was first affected in 
thirteen cases; in three cases husband and wife simul¬ 
taneously ; in one the woman was affected first—she was a 
“ puella publica.” The proportion showing a history of 
syphilis is not reliable, owing to the fact that the notes were 
made at different times by many observers. The statistics 
are, however, of interest, as showing that the husband is 
almost invariably affected first; and that the proportion of 
married couples affected is about 2 5 per cent. This per¬ 
centage corresponds very closely with the average number 
of persons affected with para-syphilitic affections. 

One of the cases recorded was especially instructive. The 
husband was infected in 1876. Married in 1879. The wife in 
1880 gave birth to a daughter who was syphilitic. In 1894 the 
husband first showed signs of tabes. In 1895 the daughter first 
showed signs of paralytic dementia and in 1897 the wife was 
similarly affected. 

My own cases furnish the following results of affection 
of Married Couples : 



History of Syphilis. 


Age and Onset. 

Interval between af¬ 
fection of husband 
and wife. 


Wife, Ataxy. 

Husband, Par¬ 

Miscarriages, no 
living children. 
Pigmented scar. 
Indirect from 
wife’s history. 

45. Onset with 
Charcot’s joint 
gastric crises. 
35. Death at 36. 

10 years, hus¬ 
band affected 


Wife, Tabo«par¬ 

Husband, General 
Paralysis prob¬ 
able, as be had 
suffered with fits 
and died insane. 


Husband, soldier 
in India. 

35. Optic atro- 
P h y- 

Age ? Affected' 
after his wife 
went blind. 







History of Syphilis. 

Age and Onset. 

I nterval between af¬ 
fection of husband 
and wife. 


E.E.G., Wife, 

Husband, Tabo- 

Serpiginous pig¬ 
mented ulcer on 
leg. Five still¬ 
born or miscar¬ 
riages. , Four 
children died in 
infancy. Seven 

No signs of Syph¬ 
ilis noted in hus¬ 
band, who died at 
another asylum. 

62. With men¬ 
tal symptoms. 
Came on after 
her husband 
had been 
taken to the 

60. Blindness, 
ataxy and 
mental symp¬ 

2-3 years, hus¬ 
band affected 


Wife, General Par¬ 

Husband, Tabo- 

Child by first hus¬ 
band, sterile by 
2nd (Syphilitic) 

Scar of chancre 
and indurated 
glands, papery 

35. Worried 
about hus¬ 
band. Mental 
delusions and 

41. Optic atro¬ 
phy. Ataxy, 
then mental 

2 years, husband 
affected first. 


Wife, Ataxy. 

W.F., Husband, 

One child bom 

Scar of chancre, in¬ 
durated glands. 


40. Mental 
symptoms and 

or nearly so. 


L.H., Wife, Tabo- 

Husband, General 
Paralysis or 
Pseudo G.P. 

Three miscar¬ 
riages, said her 
husband gave 
her Syphilis. 

53. Mental 
symptoms and 

54. Dementia. 
Spinal affec¬ 
tion and pare¬ 

1 year after hus¬ 


Wife, General Par¬ 

E.C.B., Husband, 
General Par¬ 

Syphilitic psoria¬ 

Leuco - placia. 
Gumma of ton¬ 
gue. Indurated 


52. Grandiose 
delusions, de¬ 
mentia, pare¬ 

Wife admitted 
to Cane Hill 
one year after 
husband had 
been admitted 
to Claybury. 

In all these cases it is probable that the husband 
infected the wife. In only three cases were the husband 
and wife both seen. In the remaining four one or the other 
was seen personally. In all seven it may be presumed that 
the husband suffered with syphilis and infected the wife; 
in five out of the seven the symptoms commenced certainly 



in the husband first. Syphilis, or signs of it, were observed 
or indicated in either husband or wife in every case with 
the possible exception of Case 64 (vide p.-m. notes), but 
the chances of a man being infected who has been a 
soldier and served in India 1 are very great. 

The above cases I have merely come across while 
making this research on tabo-paralysis, but probably a 
careful analysis of all the general paralytics admitted into 
the London County Asylums would show, like Moenke- 
moller’s statistics, conjugal affection in about 2 to 3 per 
eent. of married general paralytics. This conjugal affection 
becomes an important argument in favour of (1) the 
syphilitic origin of the disease; (2) the effect of mental 
strain and worry in inducing the disease in one of its several 
forms ; (3) the fact that one of the pair may be affected with 
tabes and the other with paralysis or tabo-paralysis, support¬ 
ing the view of the unity of the two diseases engendered by 
the action of the syphilitic poison. 

In the juvenile form of general paralysis I have found 
six out of thirty-two in which one or other of the parents 
had died of the same disease; in at least 80 per eent. of 
these thirty-two cases, there were signs on the body or a 
definite history pointing to congenital syphilis, and in the 
remaining 20 per cent, it was so probable that one might 
conclude that probably every case was of a syphilitic origin. 
Dr. Tredgold found among his imbecile oases six juvenile 
paralytics, and all of these were syphilitic cases. Seeing 
that sexual excesses, alcoholism, and other causes to whioh 
general paralysis is attributed must play quite a subordinate 
part in these cases, it must be assumed that inherited 
syphilis is the essential factor. Three of the total juvenile 
general paralysis cases (about 10 per cent.) were of the 
ataxic form, and a considerable number commenced with 
optic atrophy and blindness long before the mental symp¬ 
toms developed. 

Occasionally one member of a family suffers with tabes 

•Venereal Diseases in the British Army, B.M.J.y July 27, 1901. The 
Secretary of State for India said that 522 per 1,000 of the British Arifty had 
been admitted into hospitals for venereal diseases in 1895, 313 per 1,000 in 



and another with general paralysis, e.g. (1) two brothers 
in two instances; (2) brother and sister in one instance; 
(3) father, general paralytic; child, congenital syphilis and 
tabes with optic atrophy. Cases such as these indicate att 
hereditary soil, or temperament, suitable for the poison to 
act in producing the degenerative process. 

In two of my cases of tabes there was a history of 
congenital syphilis, and in one at the age of twenty, optic 
atrophy and absent knee-jerks appeared, which suggested 
congenital syphilis as a cause, although there was no history 
of it (vide Case 1). 

Bemak has described three cases of tabes in children; 
in two there was certain hereditary syphilis, and in one 
probable; the father of the third likewise had tabes. 

Goldflamn has described one case of acquired syphilis 
which developed tabes and also had several children who 
suffered from the disease. Strumpell described tabo- 
paralysis in a 13-year-old girl with hereditary syphilis. 
Gowers’ two cases had both hereditary syphilis. Mendel’s 
two cases both hereditary syphilis. Fournier described 
four cases, certain syphilis in one, and probable in the other 
three. Bloc and Gilles de la Tourette each one, with certain 
syphilis; and Erb three pairs of sisters, six cases of tabes in 
all, in whom hereditary syphilis was demonstrable,' Gowers, 
Fournier, Baymond, Homen and others have described 
cases of tabe3 in adults as the result of hereditary syphilis, 
and Nonne (“ Syphilis und Nerven System,” 1901, p. 322) 
also gives one of his own observations, which is most striking; 
as follows : “A workman aged 32, who had suffered for two 
years with lightning pains, and had never been infected with 
syphilis or addicted to drink, presented all the typical signs 
of ataxy. He had been treated in the hospital for severe 
hereditary syphilis.” I have Occasionally noticed the same 
in general paralysis commencing in adult life. In my 
Croonian lectures I remarked that it is possible that some of 
the cases occurring in adults in which no history of acquired 
syphilis can be obtained, may still owe the disease to an 
inherited taint. It is not even necessary that they should 
show external signs of syphilis, for many of the cases of 



juvenile general paralysis were proved to be born of syphilitic 
parents, although manifesting themselves no external signs 
of syphilis ; whereas their brothers or sisters might exhibit 
well marked signs. A case of general paralysis died at 
Banstead Asylum, which had previously been under the 
care of Dr. Percy Smith at Bethlehem Hospital. The 
woman had characteristic signs of general paralysis, but she 
did not manifest symptoms of progressive dementia until 
she was 30 years of age. The patient was an unmarried 
woman, and there was no reason to believe that she had 
acquired the disease. 

Post-mortem Table Besults in Reference to Syphi¬ 
litic Residua in Tabes, compared with the Post¬ 
mortem Results in Tabo-Paralysis and General 

Westenhofer examined the bodies of seventy-two cases of 
tabes at Virchow’s Institute; in 44 per cent, certain or 
doubtful syphilitic signs were observed. These results 
compare very closely with those I have obtained in 
general paralytics; for in 213 male post mortems at 
Claybury Asylum in 1900 and 1901 there were eighty-six 
general paralytics, and 45'4 of these had signs of syphilis on 
the body; in the remaining 127, 9 per cent, had certain or 
doubtful signs of syphilis on the body. In the post mortems 
made on 249 females, there were thirty-six general paralytics; 
and of them 19'5 per cent, had signs of syphilis on the body. 
Of the remaining 213, only two (less than 2 per cent.) 
showed signs of syphilis. The frequency of non-tubercular 
salpingitis in female general paralytics is also an indication 
of the greater frequency of venereal infection in these 
women. It suggests also that a number of these may be 
recruited from women who had previously led an immoral 
life. Dr. Bolton’s statistics show that out of eighteen 
general paralytics dying at Claybury fourteen (or 77 to 78 
per cent.) showed former non-tubercular tubal disease, 
whereas in ninety-two other cases only 10 or 12 per cent, 
showed former non-tubercular tubal disease. 

These results are undoubtedly favourable to the syphilitic 



view if we consider how often syphilitic lesions heal up in 
women and disappear, leaving no certain trace behind. In 
one tabo-paralytic woman there were no external signs on 
the body; she was sterile. At the autopsy I found a scar 
on the os uteri the size of a threepenny piece. 

Racial Syphilis in Uncivilised Countries in Relation 
to Tabes and General Paralysis. 

It is asserted that in countries where syphilis is extremely 
common—Bosnia, Herzegovina, Algeria, 1 Abyssinia and 
Japan 2 —tabes and general paralysis are extremely un¬ 
common or never met with. Egypt was cited formerly, but 
the statistics of Dr. Warnock, of the Abassieh Asylum, 
Cairo, show that 6 per cent, of the inmates are general 
paralytics, and in a recent report he states that syphilis is 
demonstrable in the great majority of these cases; more¬ 
over, he considers it the essential cause of the disease. 
When I visited Jamaica I ascertained that a large amount 
of syphilis existed among the negro population; it had 
become very rife since numbers of them had returned from 

1 At a recent meeting of the Soci6t4 de Neurologic of Paris, M. Scherb, of 
Algiers, gave an account of his observations on syphilis and nervous disorders 
in the Arab, made during three years* residence in Algiers. Tertiary syphilitic 
symptoms, both cutaneous and osseous, were more frequent among the Arabs 
than among the Europeans (of Algiers). The rarity of cerebral syphilitic 
accidents and of para-syphilitic manifestations (tabes and general paralysis) 
is attributed to the fact that syphilis is a disease of comparatively recent 
importation among the Arabs of Algiers, and that its stress falls with peculiar 
vehemence in the tertiary period on the cutaneous and osseous structures. 
It may be added that the people are essentially lazy, taxing their brain and 
nervous system but little, and that the organ which is thus least taxed is also 
the least exposed to the injurious effect of syphilis. The absence of a special 
predisposition produced by syphilitic or other stresses, however, is not one 
likely to persist; for with the increase of civilisation and of alooholism the 
Arab is preparing himself a neuropathic soil for the future development of 
both tabes and general paralysis. It is pointed out that other indigenous 
Semitic races (Jews) present both tabes and general paralysis not infrequently, 
and they undoubtedly present the neuropathic basis for the development of 
those affections. In the discussion following the above communication 
Professor Raymond pointed out that among the Abyssinians syphilis was not 
uncommon, but it did not produce nervous diseases secondarily. ( Brit Med . 
Journal , Sept. 28, 1901.) 

2 Dr. S. Nose, “ Beitrag zur Tabes Syphilis Frage,** Neurol Centralblatt , 
1901. Mittheilungen der Medicin Facultat der Kaiserl. Japanischen 
Universitat in Tokio. Ninety-six cases of tabes dorsalis, eighty-three males 
and thirteen females. (1) Forty-six cases certainly syphilitic = 47*9 per 
cent. ; ten cases probably syphilitic = 10*4 per cent. (2) Without demon¬ 
strable syphilitic infection (a) Without gonorrhoea twenty-four cases = 
25 per cent.; (6) With gonorrhoea fifteen cases = 16*6 per cent. 



Panama. Dr. .Henderson, of Kingston, informed me that 
tabes was uncommon; but I found at the asylums many 
cases of general paralysis; and Dr. Plaxton, the Super¬ 
intendent, told me the latter was common. I examined 
there several women suffering with this disease. 

On the other hand, in Iceland and the rural districts of 
Ireland and Sweden syphilis is very rare or unknown, like¬ 
wise tabes and general paralysis; again, the comparative 
absence of the diseases, tabes and general paralysis, in priests, 
Quakers, and women of the better classes in whom syphilis 
is rarely met with, but where all the secondary or con¬ 
tributory causes occur just as frequently as in other classes 
of society, tends to support the view that syphilis is an 
essential factor. We can only reconcile the two contra¬ 
dictory facts that races free from syphilis are free from tabes 
and paralysis, and that races extensively syphilised do not 
suffer from these two diseases, by supposing that other 
contributory factors are absent in the latter, viz., mental 
stress combined with an emotional, lustful, neurotic, neuro¬ 
pathic or psychopathic temperament, especially when 
assisted by indulgence in alcohol. Excesses in baccho et 
venere are not only powerful agents in the production of 
tabes in all its forms, but also in hastening the progress; 
exposure to cold and wet, ako injury, may act as contri¬ 
butory factors. We will now consider each of these causes 

Stress. —Prof. Edinger has emphasised the importance 
of stress in determining the seat of the degenerative process, 
and he has shown by experiment that degenerative changes 
in the posterior column of the cord can be induced in 
animals rendered anaemic by a poison like pyridin, if these 
animals are daily made to use their limbs for a certain 
time so as to produce artificially stress of the nervous 
structures concerned in locomotion. My experience cer¬ 
tainly shows some instances in which occupation has 
apparently determined the seat of the lesion. The occupa¬ 
tion of sixty successive male cases of tabes dorsalis met 
with in hospital practice or outside the asylum, showed 
only two that were not laborious, involving stress pf the 


lower limbs. There were two clerks and one of these 
suffered with cervical tabes, and in the other the arms 
were early affected and the patient subsequently became 
a tabo-paralytic case. A mounted policeman was first 
affected in the arm with which he held the reins. Two 
packing-case makers, a carpet planner, a parcel-post sorter, 
were early and markedly affected in the arms. Two tailors 
were only affected in the legs, but they worked a treadle 
sewing machine. A carpet planner who knelt all day suffered 
with tabo-arthropathy of both knee joints, whereas a stone 
mason who wielded a 41b hammer in his right hand, and a 
chisel in his left, suffered with a Charcot’s joint of the right 
shoulder and arthritis of both hands, and of the left elbow. 
Among the fifteen women a large proportion had to earn their 
living by charing, which means kneeling or scrubbing, or else 
they worked a sewing machine ; and this may account for the 
frequency with which they suffered with tabic-arthropathy 
affecting one or both knee joints. Of the fifteen women 
seen in hospital practice, seven suffered with Charcot’s joints, 
and in six out of seven it was the knee. Of the fifty-four 
men there were only five who suffered with joint affections. 
Among the tabo-paralytics, there were eighteen in which 
cord symptoms were known to have preceded mental 
symptoms, and only two of these did not follow an occupa¬ 
tion involving stress on their lower limbs. 

Mental worry and strain .—In many of the cases of tabo- 
paralysis mental worry seems to have preceded the develop¬ 
ment of the brain symptoms. Not infrequently the blindness 
from which the patient suffered was a cause. Exposure to 
cold and wet were often assigned as causes, likewise unequal 
temperature of the anterior and posterior surfaces of the 
body, as in men working at a forge, engine drivers and 
stokers, but as a rule these were only contributory factors of 
minor importance. According to Erb in only 1'4 per cent, 
of cases may exposure to cold and wet be considered primary 
causes. Injury to the spine in four cases was thought by the 
patients to be the cause of their affection; it certainly 
seemed that the disease came on after the injury, but would 
it not have done so without ? 



In all the traumatic cases save one there was a definite 
syphilitic history. Klemperer collected from various sources 
of literature, thirty cases of so called traumatic tabes, but 
Hitzig in a valuable monograph has dispossessed Klemperer’s 
inferences of much of their import. Hitzig showed that but 
few of Klemperer’s cases were genuine traumatic tabes. 
Erb gives the percentage as 0 3, Leyden and Goldscheider 
say that it is not considerable. It is true that trauma may, 
as in general paralysis of the insane, act as a contributory 

Hereditary Predisposition .—I do not think this plays 
such an important part in tabes as in general paralysis. 
Charcot, Ballet, Benedikt, and Borgherini considered it an 
important factor in tabes; Bosenblatt, Raymond and 
Fournier, Erb and Gowers as a contributory factor of some 
importance; Leyden as an effective agent. Redlich attaches 
no very important role to hereditary influence, scarcely more 
than a contributory factor. In considering hereditary 
influence we should not only take into consideration nervous 
and mental diseases in ancestors, but also temperament, 
which may mean potential neurosis or psychosis. Among 
the tabo-paralytics and tabic cases suffering with insanity 
met with in Asylums, 30 per cent, had a family history of 
insanity. In his Presidential Address to the Medico Psycho¬ 
logical Society Dr. Wiglesworth pointed out that hereditary 
influence plays a much less important part in general 
paralysis than in other forms of insanity. This was con¬ 
firmed to me by Drs. Savage, Craig, Spencer, Woods and 

Intemperance .—In twenty-six asylum cases there was a 
reliable statement obtained that the patient was not in any 
way intemperate, and it was concluded that drink as a 
contributory factor in these cases had no share. In sixteen 
cases out of sixty it was concluded that drink was a con¬ 
tributory factor of some importance; and in the remainder, 
no definite reliable statement was obtainable. In a good 
number of cases the wife’s statement was that the patient 
was a good husband and a good father. I came to the 
conclusion that drink played a more important part in 




tabo-paralysis than in tabes; but that in both it was not 
such an important factor in the production of the disease 
as in accelerating its progress. Frequently intemperance 
and lust is the first evidence met with of the degenerative 
process affecting the brain or cord. 

Mode of Onset of Tabes and Tabo-Paralysis. 

Onset of tabes dorsalis. In sixty-five cases the average 
age at which the onset of symptoms occurred was thirty- 
seven. The average interval between a definite history of 
infection and onset of symptoms was ascertainable in more 
than half of the cases, and was fifteen years. The shortest 
period was four years and the longest twenty-six. The 
average age of onset of the disease in the different decades 
was as subjoined; the age of most cases was determined 
by the history of some characteristic subjective symptom 
or group of symptoms, such as pains, double vision, visceral 
crises, or of the first objective manifestation, &c.: 

In sixty per cent., shooting pains were the first symptom 
which attracted the patient’s attention. 

In 12-3 per cent., double vision was the first symptom which 
attracted the patient’s attention. 

In 14 per cent., visceral, especially bladder troubles, and 
gastric crises were the first symptoms which attracted the 
patient’s attention. 

In 10 per cent., arthropathies or spontaneous fracture. 

In 10 per cent., failure of vision and blindness. 

The youngest age, excluding a probable congenital case, 
was 25, the oldest 55. 

Decades at which the Onset of Symptoms occurred. 

Tabes Dorsalis. 

Female General Par¬ 
alytics, 118 cases. 


1st decade.. 
2od „ 

1*5‘ per cent. 

1*75 per cent. 

6 per cent. 

3rd „ 


1-75 „ 

4 „ 

4th „ 


47-45 „ 

72 „ 

5th „ .. 



20 „ 

6th „ .. 



6 „ 

Congenital Syphilis. 



Onset of the tabo-paralytic and general paralytic cases 
was more difficult to ascertain with preciseness, because of 
the mental condition of the patients, and because of the 
difficulty to exactly fix the date of onset of mental infir¬ 
mity ; but, generally speaking, the above tables closely 
correspond, for nearly all the cases begin in the fourth and 
fifth decades, on an average fifteen years after the period of 
greatest probability of infection, viz., between 20 and 30. 
Of fifty-four cases of male tabo-paralysis, the average age 
of onset of symptoms worked out at 38£. These figures 
were raised quite one by the existence of a man and his 
wife whose symptoms (sufficient to attract attention) ap¬ 
parently only commenced at 62 and 63 respectively. The 
interval of time between infection and onset of symptoms 
could only be precisely ascertained in fourteen cases; this 
was partly due to the unreliability of the answers given 
owing to the mental condition of the patients, and partly, 
as in the spinal tabetic cases, to the fact that the patients 
denied, or did not know that they had had syphilis, although 
there was positive evidence on the body. The shortest 
interval was six years, the longest twenty-five; average, as 
in tabes dorsalis, fifteen years. 

An argument that is frequently used against syphilis 
being the cause of tabes or general paralysis in one of these 
many different clinical types is the fact that there are not 
more prostitutes affected. Since the great bulk of the cases 
occur, as we have seen, in the fourth and fifth decades, 
when it is not so easy for a woman to earn her living by 
prostitution, she is not described as such upon entering the 
asylum ; and I have found a number of such women in the 
asylums calling themselves married women, or as following 
some occupation. Occasionally, indeed, they are described 
as single women, and in many instances it is subse¬ 
quently proved (as Case 31) that they have led an immoral 

Kron’s observations upon 184 public prostitutes showed 
five with tabic symptoms at ages of 27, 28, 47, 47, and 65. 
But if one reckons only with those over 25 years of age, 
which allows nine years for the onset of the disease after 




infection, there were only thirty-six women, and of these 
five suffered with tabic symptoms; or 14 per cent, of 
syphilitic prostitutes suffered with tabes, which is far from 
a low average. (“ Ueber Tabea Dorsalis beim Weiblichen 
Geschlecht,” Deutsch. Zeitschrift fur Nervenheilkunde, 
Bd. xii., 1898.) 

In thirty-four cases it was possible to determine the 
age of onset of the spinal and mental symptoms respec¬ 
tively. Average age of onset of spinal symptoms, the most 
frequent being lightning pains, was 37£; average age of 
onset of mental symptoms was 39£. Probably this is too 
late by several years, for early slight changes of character, 
irritability of temper, moroseness, &c., are easily overlooked. 
The longest interval between optic atrophy and mental 
symptoms was eighteen years. In one half of the cases the 
spinal and mental symptoms were apparently simultaneous, 
and the cases frequently, but by no means invariably, ran 
a rapid course; in some instances they terminated fatally 
within six to eighteen months of onset of symptoms. In 
forty-eight cases it was possible to determine whether the 
spinal signs and symptoms were observed first, simultane¬ 
ously with, or successive to, the mental symptoms. In 
twenty-four cases signs of brain affection either preceded or 
were simultaneous with signs of affection of the cord or 
eyes, or both. Fournier (“Affections Parasyphilitiques, 
Tabes et Paralysie Generale,” p. 213) says: “ Tabes and 
general paralysis will be different expressions of one and the 
same morbid entity.” He further on asks the question, 
“ Is one authorised to fuse into a single morbid entity tabes 
and general paralysis?” He sums up the identical relations 
of the etiology, the close relationship and overlapping in the 
symptomatology and pathology, and destines them one day 
or other to be grouped in a single pathological entity. 

The foregoing pages on the etiology of spinal and cere¬ 
bral tabes, clinically distinguished as tabes dorsalis and 
general paralysis of the insane, tend to show that, patho- 
genetically, the two diseases are identical. I will next 
endeavour to show a close clinical and pathological rela¬ 
tionship of the different types of a single pathogenetic 
morbid entity. 




The fundamental symptoms and signs of tabo-paralysis 
and of tabes are :—(1) Reflex pupil rigidity ; (2) Lightning 
pains ; (3) Absence of deep reflexes; (4) Visceral disturb¬ 

ances, bladder troubles, and gastric crises ; (5) Disturbances 
of sensibility; (6) Motor disturbances; (7) Mental dis¬ 

A diagnosis can be made, if the pupil rigidity exists, 
combined with any of the others, for, practically speaking, 
reflex rigidity of the pupils to light and pain exists only in 
tabes, general paralysis, and acquired or congenital syphilis, 
of which (as pointed out by Sir William Gowers) it may be 
the sole sign. Very rarely cases of focal cerebral lesions 
may be accompanied by Argyll-Robertson pupils, especially 
lesion of the corpora quadrigemina. Some authors point 
out that in alcoholism and other diseases reflex rigidity of 
the pupils may exist, but these are cases complicated by 
syphilis. Indeed, the existence of reflex rigidity of the 
pupils is evidence that a mania a potu is due not only to the 
toxic effects of the alcohol, but also to general paralysis. 
The value of this sign is shown by the fact that in thirty- 
two cases of tumour cerebri found on the post-mortem table 
at Claybury, the notes showed that in only one case was 
there reflex rigidity of the pupils to light, and this was a 
syphilitic case with general paralysis. Yet on account of 
progressive dementia and other mental symptoms, and not 
infrequently failure to discover or even absence of the cardinal 
symptoms of tumour (optic neuritis, headache, and vomit¬ 
ing), more than one half of these cases were diagnosed as 
general paralysis. As a rule, we do not know how long the 
Argyll-Robertson pupil has been in existence, for, of course, 
the patient is unaware of its presence, and only comes under 
observation when some other early symptom such as pain, 
a fit or mental symptoms, double or defective vision, visceral 
crises, or ataxy brings him to the doctor. 

Eye Symptoms of Tabes and Tabo-Paralysis. 

Pupil changes are met with in nearly all cases of tabes 
and tabo-paralysis, and in the majority of cases of general 



paralysis, in the earlier or later stages of the disease. 
The hospital cases of tabes closely correspond to the asylum 
cases of tabes and tabo-paralysis as regards pupil phen¬ 
omena, as the subjoined statistics show. 

Tabes (Hospital Cases). 

Tabes or Tabo-Paraly- 
sis (Asylum Cases). 

73*5 per cent. Argyll-Robertson pupils on both sides 
3 „ „ „ one side 

3*7 „ sluggish to light 

15 ,, inactive to light and accommodation 1 

70 per cent. 







Occasionally in tabes and more often in tabo-paralysis 
and general paralysis, paradoxical reaction to light occurs; 
viz.: on removal of the shadowing hand no reaction 
takes place for a second or two, then the pupils dilate 
slightly. Mobius explains this phenomenon thus: that 
probably during the process of covering the eyes, the patient 
is accommodating, and when the shadowing hand is removed, 
accommodation is relaxed, the process of accommodation 
being a slower process than the light reflex. A sluggish 
reaction to light is not necessarily pathological, and unless 
there is a difference between it and accommodation, it may 
be of no import. With absence of the light rigidity, there 
is nearly always absence of reflex cutaneous pain, and it 
is not uncommon to see a patient suffering agonising pain 
with pin point pupils. 

Inequality, Irregularity and Size of Pupils. 

Before the discovery of the Argyll-Robertson phe¬ 
nomenon, inequality of the pupils afforded a valuable 
sign of the disease ; likewise very small pupils ; and even 
now such alteration may attract the physician’s attention, 
and lead to his making a more careful examination of a case 
which presents urgent symptoms pointing to organic disease 
of internal organs ; e.g., in Case 7, which was admitted for 
acute intestinal obstruction, the surgeon who was called in 
to operate had his attention attracted to the very small 

1 Most of the cases which were totally inactive to light and accommodation 
were the subjects of complete optic atrophy. 



pupils, while the man' was suffering agony, and this led to 
the discovery of the true nature of the disease. Inequality 
of the pupils is more frequently met with in tabo-paralysis 
and general paralysis than in tabes. 

Size, Inequality, Irregularity of Pupils in Tabes 

Size, Inequality, Irregu¬ 
larity of Pupils in Tabo- 
Paralysis (Asylum). 

Unequal 1 


40 per cent. 

... 65 per cent. 


... ... 

18-5 „ 

... 27 „ 


32 „ 

... 33 

Pin Point 

... ... 

18 „ 

... 16 

Medium ... 

... • • • 

34 „ 

... 33 ,, 

Large on one or both sides 

16 „ 

... 18 

Paralysis of the external ocular muscles may be transient 
or permanent. Diplopia (double vision) is often the first 
subjective symptom which attracts attention ; but it may be 
due to a syphilitic meningitis. In several of my cases it 
occurred within a few years of the syphilitic infection, but 
as a rule the interval is much longer. Any muscle may 
be affected, but the external rectus is the most frequent. 
The patients often complained of double vision, which lasted! 
a few days or weeks, for which they attended an eye hospital 
long before the other symptoms troubled them. Some ol 
these cases were sent on to me from the Westminster 
Ophthalmic Hospital, or by my friend, Mr. Treacher Collins, 
from Moorfields. 

Ocular paralysis in the hospital cases, a considerable number 
of which, however, were sent from the eye hospitals, render the 
following statistics much too high. 

In twenty-two there was double vision of a transitory nature; 
it was, in nearly all the cases, a very early symptom. There were 
nine cases of ptosis (in four associated with squint) and four of 

1 These figures are only approximate, as a number of cases were only seen 
once or a few times. The series contained a considerable number suffering 
with optic atrophy or blindness. Irregularity of the pupils may occur 
independently of synechiee, the pupil being angular, elliptical or oval; it was 
more frequently met with in the asylum than hospital cases. The asylum 
oases, as a whole, came more frequently under my observation, and I was 
able to note the fact that the degree of inequality varied considerably and, my 
impression is, much more frequently than in the hospital cases of Tabes. Not 
infrequently a small pupil became large or medium-sized, and this often 
occurred during or after a series of fits. Frequently pupils which on the one 
hand were equal at one period of the disease, became unequal, while on the 
other hand, pupils which were unequal might become nearly equal. 



nystagmus. In eleven cases there was permanent ocular 
paralysis, four partial of 3rd, one of 4th, five of 6th, one ophthal¬ 
moplegia interna and externa bilateralis. 

Among the asylum cases, paralysis of the ocular muscles was 
much less frequently met with. In only eight was double vision 
described as an early symptom (13'3 per cent). In three cases 
transitory diplopia occurred while the patient was in the asylum. 
Permanent ocular paralysis occurred in four cases, two unilateral 
ptosis, and two unilateral 6th nerve paralysis. 

Atrophy of the optic nerve is one of the most serious 
symptoms that can arise in tabes; it is an early, indeed a 
very early symptom, and the defect of vision or blindness 
may be the first cause of the patient seeking advice; its 
frequency is difficult to ascertain. Sir William Gowers 
states that one in ten cases suffers with it; according to 
Leimbach it may be the first symptom in 1*5 per cent. 
Among my sixty-five hospital and infirmary cases, there 
were twenty with optic atrophy and ten of them were 
completely blind. A great many of them remained in the pre- 
ataxic stage many years (vide Cases 1, 61); others became 
general paralytics and died. The large number of these 
cases was due to the fact that a considerable number were 
sent to me from Ophthalmic Hospitals. Again, if we took 
infirmary cases it would hardly be fair, because blindness 
leads to incapacity to earn a livelihood. When, however, 
we come to consider asylum cases we find that it is 
extremely common in tabo-paralysis; owing, however to the 
difficulty in examining these patients ophthalmoscopically a 
few cases may be overlooked, but 35 per cent, of the sixty 
cases were found to have well marked optic atrophy, and 
50 per cent, would probably be nearer the mark, for I have 
found often, post mortem, optic atrophy which was not noted 
during life. In 150 consecutive cases of general paralysis 
found on the post-mortem table at Claybury, the optic nerves 
were carefully examined, and naked eye atrophy was found 
in only 7 per cent.; several of these belonged to the juvenile 
form of general paralysis (in which it may occur indepen¬ 
dently of any degeneration in the posterior columns of the 
spinal cord), the remainder belonged to the tabetic form of the 



disease in adults, as ascertained by microscopical examination 
of the spinal cord. Optic atrophy, then, occurring in tabes 
is to my mind, apart from the blindness, a serious indication 
of the possibility of the degenerative process attacking the 
brain. My experience would lead me to believe that the 
mental worry occasioned by the blindness in a few instances 
tended to bring this about. The failure of vision usually 
commences with limitation of the peripheral field of vision 
in one eye and loss of colour vision; then the other is 
affected, or both may be affected simultaneously. The onset 
is usually gradual and the course slowly progressive, but 
sometimes the sight is lost, apparently in a few days, or 
almost suddenly. Doubtless in some of these cases there 
has been loss of the peripheral field of vision with the 
retention of central acuity, and it is the comparatively 
sudden destruction of the remaining fibres to the macula 
which leads the patient to believe he has suddenly lost his 
sight. It may, however, be (as Gowers suggests) due in such 
cases to an interstitial inflammatory process, but ophthalmos¬ 
copic examination shows no change to account for it. 

Dr. Wiglesworth was one of the first in this country to 
call attention to optic nerve atrophy preceding the mental 
symptoms of general paralysis of the insane. In conjunction 
with'Mr. Bickerton, he described the optic nerve changes 
met with in a series of sixty-six cases of general paralysis. 
They showed that while in the majority of cases of this 
disease the fundus oculi presented a normal appearance, in a 
considerable minority changes in the direction of neuritis or 
atrophy were found. 

The credit of first describing the form of tabes known 
as optic tabes is due to Benedikt, who stated in 1881 
that the abortive cases of tabes {formes frustes) are the ones 
in which optic atrophy is a prodromal symptom. 

In 1887 Benedikt stated a law, from which he knew no 
exception, that the tabetic motor symptoms, no matter what 
development they may have reached, vanish as soon as optic 
atrophy appears. Dejerine points out that this latter state¬ 
ment is not true and I certainly agree with him, vide (among 
many others Case 28.) I would go further and say that 



it has no influence upon the ataxy, when it arises in a 
patient already in the second stage of ataxy; in this respect 
it agrees with the fact that cortical degeneration occurring 
in an advanced case of tabes with well marked ataxy does 
not cause the disappearance of the ataxy, although the 
advent of dementia and other signs of cortical degeneration 
like optic tabes certainly arrests the spinal degenerative 
process and modifies ataxy of the first degree. An ex¬ 
planation of these facts is attempted in the chapter on 
“Inco-ordination.” Dejerine states that the number of cases 
of tabes with blindness in which the disease does not 
progress beyond the pre-ataxic stage is considerable. He 
and Martin studied 100 tabetic cases at Bicetre, eighteen of 
whom were completely blind, and none of these presented 
motor disturbance. According to my experience lightning 
pains usually precede optic atrophy, but not invariably. 
Usually when the optic atrophy occurs early, the lightning 
pains diminish in intensity, and even at times disappear. 

An important point to remember is the frequency with 
which optic atrophy is followed by tabo-paralysis; in quite 
50 per cent, of the cases of this form of the disease met with 
in asylums (and they are fairly numerous), the cerebral 
symptoms followed optic atrophy and blindness. In many 
instances the mental trouble occasioned by the blindness 
and loss of livelihood undoubtedly acted as the exciting 
cause of the brain degeneration. 

Patients with paralytic dementia on the one hand, do 
not as a rule suffer with visual hallucinations, except in the 
acute maniacal condition, especially that accompanied by 
alcoholism. Cases of tabo-paralysis, on the other hand, with 
optic atrophy frequently have visual hallucinations {vide p. 79.) 

Sir William Gowers states that Charcot believed that 
nearly all cases of so-called simple primary optic atrophy 
develop finally spinal symptoms, and he reports a case in 
which amaurosis lasted twenty years before any other 
symptom of tabes was noted ; in another case sixteen years 
passed before distinct signs of tabes occurred. Every case 
of optic tabo-paralysis that I have examined post mortem, 
although many of them showed no ataxy during life, yet 



presented upon microscopical examination well marked 
degeneration of the posterior columns due to degeneration 
of the exogenous system of fibres, and corresponding atrophy 
of the posterior roots {vide Cases 61-63). 

Section II. 

Sensory Disturbances. 

Sensory disturbances are either subjective or objective, 
and these again are of two types: (1) destructive, causing 
loss of function ; (2) irritative, causing abnormal or perverted 
function. The sensory disturbances relate to common 
sensibility of the skin, viz. : thermal condition, pain and 
pressure, or to the special senses, especially the complex of 
sensations termed “ kinsesthesis ” or muscular sense of 
Bell. The clinical phenomena of tabes, and, in a measure, 
of tabo-paralysis, are due to these disturbances. Although 
there is a symptomatic similarity among all the cases by the 
more or less constant presence in some stage of the 
disease of certain sensory disturbances, e.g., lightning pains, 
anaesthesia or analgesia, which are the best examples of the 
two types, there is hardly ever identity of symptoms, and 
no two cases are exactly alike. The complexity of the 
symptomatology agrees with the polymorphic character of 
the lesions. A study of the microscopic changes in the 
peripheral and central nervous systems in a large number 
of these cases explains this general uniformity and special 
diversity of the symptoms. The fact that changes always 
occur in the posterior spinal roots and their projections in 
the cord explains the general uniformity in the objective and 
subjective sensory disturbances of the skin, muscles, and 
joint structures, whilst the variability of distribution and 
extent of the morbid process in thirty-two posterior roots, 
and their projections in the cord, as well as the variable 
degree of complication by lesions of the peripheral afferent 
nerves, explains the frequent diversity of precise distribution 
of the anaesthesia, analgesia, hypersesthesia, hyperalgesia 



met with. The sensory dissociation shows that certain 
fibres subserving special functions are particularly affected, 
e.g., the muscular sense-fibres of the lower limbs, and 
the nerve-fibres innervating joint structures; again the 
light tactile anaesthesia of the mid-thoracic region, without 
analgesia, shows that the disease process is selective, and is 
related to the intraspinal terminations of the roots and not 
the peripheral nerves. For, in a neuritis, the sensory 
symptoms have not this dissociation, nor this distribution. 
The existence of these sensory disturbances in the insane 
tabetic, helps to explain many of their delusions and illusions, 
e.g., the idea that enemies are torturing them with electricity 
(it was hot irons and pincers before electricity was in 
general use). 

The subjective disturbances of the nerves of special 
sense and of the viscera are still more liable to receive an 
insane interpretation, and give rise to delusions and illu¬ 
sions. There is a definite relationship between the degree 
of ataxy and the reflex spinal tonus, which is due to partial 
or complete abolition of the intraspinal paths conducting 
afferent impressions from the muscles, tendons, and struc¬ 
tures around and within the joints, and this is due not only 
to the withdrawal of the guiding sensations, but also to 
muscular hypotonus. 

The skin sensibility was tested in forty-eight successive 
cases of tabes and a number of cases of tabo-paralysis, and 
mapped out on charts; the distribution was subsequently, 
when the series was completed, compared with the root 
distribution given by Seiffer, which is based upon an 
analysis of the researches of Head, Thorburn, Kocher, 
Starr, and Wichmann. From thirty-two cases where root 
distribution was sufficiently definitely determined as regards 
tactile anaesthesia, a composite chart was made. 

Method of Examination. 

Anaesthesia to light tactile sensations was made by 
touching the patient very lightly with the tip of the finger, 
analgesia by pricking with a needle, and heat or cold by a 



test-tube filled with ice or hot water. The patient’s eyes 
were covered with a towel. Twelve of these cases were care¬ 
fully noted by my clinical clerk, Mr. J. P. Candler, who 
embodied the results in a thesis. Most of these, however, 
I myself have verified. The distribution and character of 
the sensory disturbances, when combined with a careful 
examination of the spinal cord and roots, will help to throw 
some light upon the conduction of various sensations in the 
cord, the functions of various tracts and groups of fibres, 
also the inflow of visceral sensations by the white rami. 
The spinal cords which I have systematically examined so 
far have been mostly obtained from the cases of tabo- 
paralysis or cases of tabes in which the sensory disturbances 
were not accurately determined during life, owing either to 
mental disturbances, or to the fact that they died before I 
commenced these researches of the accurate distribution of 
the sensory disturbances. Before passing to a description 
of my own observations, I will give a brief description of 
the results of other observers. 

Duchenne, “ Trait6 d’61ectrilization localizes,” 1872, devotes 
a few lines to the sensory manifestations of tabes. He mentions 
that in the second period of the disease abolition of tactile and 
painful sensibility occurs. The sensibility of the feet and hands 
is in general more or less diminished, especially the palmar and 
plantar surfaces following the appearance of troubles of coordina¬ 
tion of movement. In the skin the painful and tactile sensibility 
are simultaneously damaged, but more often painful sensibility 
is intact or little altered, and temperature is last affected. 
Duchenne, therefore, noted the sensory dissociation, although he 
was incorrect in several other ways. 

Topinard, “ De l’ataxie locomotrice,” 1864, also Cruvielhier 
had noticed this sensory dissociation. 

A most valuable paper has recently appeared by Forster and 
Frankel. 1 These authors give an admirable summary of the work 
of previous observers before describing their own observations. 
They point out that Oulmont in Charcot’s Clinique was the first 
to show that the statement of Duchenne regarding the fact that 
the objective disturbances were most constant in the extremities, 

1 “ Untersuchungen iiber die Storungen der Sensibilitat bei der Tabes dor¬ 
salis” von Dr. Friinkel und Dr. Foerster. Archiv f. Psychiatrie mid Nerven- 
Jtrank. Band 33, Heft 1. 



was incorrect. Oulmont examined twenty tabetic women and 
fdund sixteen cases of trunk disturbances of sensibility. These 
disturbances were especially localised between the nipple and 
umbilicus and characterised by their symmetry. 

The essential subjective phenomenon is girdle-sensation, and 
below the girdle of anaesthesia (at least in front) is a zone of 

Hitzig first emphasised the great frequency, and above all the 
diagnostic importance, of these sensory disturbances of the trunk. 

Lahr, whose researches include sixty tabetic cases, found 
sensory disturbances of the trunk fifty-five times. The five cases 
where these sensory disturbances were absent were five tabo- 
paralytics, with only slight but nevertheless distinct spinal 

Summary of Lahr's results : 

(1) Hyperaesthesia appears to be a regular and generally early 
sensory disturbance of tabes. # 

(2) The sensory disturbances for a long time consist only of a 
diminished sensibility for light tactile impressions, whilst, as a 
rule, in the legs there is at the commencement only a diminution 
of painful sensations and of the sense of position. The latter 
generally appears to precede the trunk hyperaesthesia. 

(3) The localisation in the trunk usually corresponds to the 
distribution of the middle or lower dorsal nerves. Their further 
distribution follows generally pretty symmetrically the encircling 
horizontal zone of the trunk, which extends upwards and down¬ 
wards and in a characteristic manner, to the arms. In sixteen 
cases it spread to the arms, first to the axilla, then to the ulnar 
side of the arm and lastly to the radial. 

(4) The extent of this tactile anaesthesia is quite characteristic, 
it corresponds not to the area of distribution of the peripheral, but 
to that of spinal roots and their intra-medullary projection fibres. 
It is not, however, contended that the peripheral nerves may not 
be affected. 

(5) A wide-spread hyperalgesia, especially for cold, occurs in 
the borders of the hyperaesthetic or anaesthetic areas and between 
the zones affected; and the reflex excitability of the skin is here 
very lively. In the hyperaesthetic and anaesthetic area it may be 
lowered or lost. 

(6) Sensory irritation phenomena are very common, but not a 
regular accompaniment of the anaesthesia. Ulnar compression 
causing no tenderness appears as a rule in tabes in conjunction 
with other demonstrable sensory disturbances. 



This admirable piece of work by Lahr was an important addi¬ 
tion to our knowledge of the sensory disturbances of the trunk 
and especially to the localisation of the sensory disturbances in 
the upper extremity. Lahr also pointed out the existence of 
perfectly normal areas of sensibility lying between hyperaesthetie 
or anaesthetic areas. 

Chipault’s researches on the topography of sensory disturbances 
in fourteen cases of tabes showed similar results to those of Lahr. 

These areas according to Chipault are especially the seat of 
sensory anomalies, the trunk, the arms, the legs. In more than 
one-third of his cases there was a continuous sensory disturbance 
of arms, trunk and legs, which is in opposition to the results of 
Lahr, Forster and Frankel. 

Probably his series included a large proportion of cases in the 
third paralytic stage. He lays stress on the coincidence of the sub¬ 
jective phenomena, pains and paraesthesia, with the objective 
demonstrable anaesthesia and analgesia of the several areas. 

Patrick made observations especially upon the trunk-anaesthesia, 
and he called attention to the fact that in the trunk there occurs 
almost always only pure tactile anaesthesia, which is consequently 
regarded by him as a special sensory disturbance. He also 
pointed out that unaffected areas lie between affected ones. 

Hintze described trunk anaesthesia in six out of seven cases. 

Marinesco examined fifty cases in the cliniques of Raymond, 
Marie, and his own at Bucharest with the following results. 
There are four principal regions in which there are light tactile 
disturbances of sensibility. 

(1) Thoracic.—Forty out of fifty cases. 

(2) Genito-perineal.—Under side of scrotum and later the 
whole scrotal regions, in well marked cases, also the penis. Less 
frequent in the region of the anus. 

(3) Region of the upper limb, ulnar side. 

(4) Region of the lower limb. 

It is difficult to estimate a precise type for the lower limbs, 
for here are the greatest variations. Four regions correspond 
to well-pronounced sensory subjective disturbances : anaesthesia 
of the thorax to the girdle sensations: genito-perineal to impotence 
and rectal crises; anaesthesia on the inner surface of the arm to 
the ulnar sensation ; lastly, anaesthesia of the lower extremities to 
the lightning pains, and paraesthesia. 

Forster and Frankel. These authors give a brief description 
with charts of fifty cases especially relating to sensgry disturbances 
of the skin, joints and muscles. Their conclusions are as follows : 



(1) No single case of tabes with ataxy in which the sense of 
position of joint was not affected. The authors speak of it as 
joint sensibility. 

(2) Generally speaking, there is a parallelism between the 
sensory disturbance and the ataxy, but individual differences 
may exist according as the cerebrum reacts to the imperfect 
sensory stimuli. The degree of ataxy may not be the same in 
the two limbs, and the joint sensibility will then be more impaired 
on the side most ataxic. 

(3) As a rule, the disturbances are most marked in the joints 
of the toes and ankles; but sometimes they may be more marked 
in the joints of the hips and knee. 

(4) They call attention to the great frequency of the joint 
sensory disturbances in the upper limb, generally not marked, and 
much less (usually) than in the lower. When the case is one of 
arm tabes, shoulder, elbow, and wrist are affected ; otherwise 
only the fingers (twenty-three times out of thirty-two tested 

(5) They determined the loss of sense of fatigue in five cases. 

(6) Skin Sensibility . In not one of the forty-nine cases studied 
could the skin sensibility be considered normal. In all but five 
of thirty-eight cases in which there was light tactile sensory dis¬ 
turbance, there was also present disturbance of painful sensibility. 
In the remainder there was a disturbance of painful sensibility. 

Topography of disturbances of skin sensibility :— 

Sensory disturbances were found in the face in six cases 
arising at all stages of the disease. In one case, the one half of 
the tongue and the mucous membrane of the mouth on one 

Sensory disturbances of the trunk occurred in forty-five cases 
out of forty-nine ; in one case the patient was in the pre-ataxic 
stage. The anaesthesia generally begins above the axilla and 
extends forwards through the nipple to the middle line. The 
upper and lower borders are horizontal, uniform lines, but con¬ 
siderable deviations from this, the usual form, may exist, there 
being occasionally only islands of anaesthesia or hyperaesthesia. Out 
of thirty-eight cases in which light tactile disturbances were dis¬ 
covered, in only eight was analgesia or blunting of painful sen¬ 
sation found. Loss of painful sensation of trunk is later than 
light tactile sensibility, and in only a single case did they find the 
area of painful sensation more extensive than that of tactile. In 
four cases the anesthetic area was hyperanalgesic. Very fre¬ 
quently there was an increase in the sensory excitability in the 



neighbourhood of the anaesthesia. Hyperaesthesia of the trunk 
for cold was frequently present, also sensory disturbances of the 
upper extremity. 

In thirty-seven cases out of forty-nine the arms were affected. 
The anaesthesia was continuous with the trunk anaesthesia, and 
extended as a streak along the inner side of the arm, limited 
sometimes to the upper arm and often extended to the fore-arm, 
and not infrequently to the inner side of the ring finger and the 
whole of the little finger. It may extend to the whole fingers, 
but very rarely affects the whole arm. The sensory disturbance 
is usually anaesthesia or hyperaesthesia. 

Sensory disturbances of the lower extremity :— 

In forty-four out of forty-nine cases there were disturbances 
of sensibility in the lower extremity ; in eighteen of these, dis¬ 
turbances round the anus. In all cases the sensory disturbance 
was analgesia or hypalgesia, and if tactile disturbance was 
present, it was usually less extensive than the analgesic area, 
thus contrasting with the sensory disturbance met with in the 
trunk and upper extremities. Disturbances of heat and cold 
sensations are rare. 

Having thus given a brief account of previous observations, 
I will now proceed to give the results obtained in my own 

Subjective Sensory Phenomena of Tabes and Tabo- 


Lancinating Pams .—The pains of tabes are variable in 
intensity, situation and duration. The patient usually 
has suffered months or years before their true nature is 
discovered. They may be slight or severe, generally occurring 
in paroxysms, and are likened to stabbing, shotting, boring, 
or lightning, or to hot wires thrust into the flesh. A patient 
may be free from pains for hours, days, weeks, or even 
longer; they may last a few minutes and then cease, to 
recur again in the same situation or in another. The 
attacks of pain may last a day, a day and night, or several 
days, causing the patient the greatest suffering and agony, 
relief being obtained only by morphia. Rarely does the pain 
correspond with the distribution of the nerve, although a 
patient may come thinking he is suffering with sciatica. 
The seat of the pain is most varied. It may start in the 



great toe, and the patient thinks he has gout; it may start 
in joints and be attributed to rheumatism ; or it may be felt 
in the skin or muscles. The skin is usually hyperaesthetic 
over the seat of the pain, whether it be superficial or deep, 
and this hyperaesthesia may last after the pains have ceased. 
Herpetic eruptions follow in very rare instances, for I have 
only met with one case in sixty, and that subsequently 
turned out to be a tabo-paralytic. In one case of tabo- 
paralysis symmetrical bullse occurred in the limb and 
trunk. Examination of the peripheral nerves showed acute 
degeneration of the fibres, proceeding to the skin area of the 
bullse. Also acute degeneration changes in the cells of the 
corresponding spinal ganglia. In another patient erythema¬ 
tous patches occurred after an attack of pain in the arms. 
Some patients complain of pain running in the long direction 
of the limbs, which they mistake for sciatica. When pain 
occurs in the trunk it is frequently unilateral, and not 
uncommonly accompanied by gastric crises. The girdle 
pain is frequently experienced, and a tightness compared to 
an iron jacket or the constriction of a tight belt has been 
complained of. The pain running down the inner side of 
the left arm might be mistaken for angina. Very often the 
pains radiate all over the body, and quite a number of 
patients who suffered with gastric crises said that with the 
attacks of vomiting, pains started from the mid-thoracic 
region and radiated all over the body with the exception of 
the face. One man pointed out that the face was unaffected, 
except in an area which corresponded to the distribution of 
the second cervical root (vide fig. 1, p. 47); another, a woman 
(Case 17), suffered so severely that she could hardly bear the 
touch of the bed-clothes, and even the light of the windows 
was so painful she would bury her face in the pillow; the 
only part of the body where she did not suffer the severe 
pains during these crises was the left leg below the knee. 
The right leg had been amputated above the knee for 
Charcot’s joint. The left leg, in which the pains did not 
radiate, was absolutely analgesic and anaesthetic below the 
knee. This would rather indicate that the sentient gray 
matter subserving painful sensation for this leg or the intra- 



spinal terminals of the posterior spinal neurones had been 
completely destroyed, therefore painful sensation could not 
be projected outwards into the limb. That this is a more 
likely explanation than destruction of the peripheral nerves 
is shown by the fact that pain of central origin may be 
referred to a limb which has been amputated. 

Another case was interesting as showing that a toxic 
condition of the blood may set up crises and attacks. This 
patient (Case *20) had a discharging sinus from a suppurating 
Charcot’s joint; she volunteered the statement that when 
pus accumulated owing to the sinus getting blocked, she 
was pretty sure to have an attack of vomiting associated 
with severe pain. 

In the tabo-paralytics or tabetics with mental symptoms 
these attacks of pain may be insanely interpreted. They 
are, therefore, rather illusions than delusions. These 
patients often believe they are being tortured by unseen 
agencies, that electricity has been turned on by their 
enemies; they have been given poison which has gone into 
their legs and feet (as Case 66). They may associate the pains 
experienced with dreams or visual hallucinations; and they 
may tell you (as in two cases) that lions and wolves came 
and gnawed their limbs by night, and will beg you not to 
let them be tortured again. The pains may last during the 
whole course of the disease, but frequently in the third stage 
of the disease, when the roots which are undergoing degener¬ 
ation have become completely destroyed, the pains abate or 
cease; that is if the disease does not steadily spread up to 
affect the arms. In tabo-paralysis dementia is usually 
associated with abolition of the painful sensations caused by 
pricking, and the patient as a rule does not complain 
of attacks of pain or torture ; in this respect, markedly 
differing from the tabetic with delusional insanity, who 
probably suffers more than the sane tabetic, as he is not only 
tortured with physical pain, but also with delusions of perse¬ 
cution by unseen agencies—the true pains forming a realistic 
basis to the delusions around which his whole psychical 
existence may centre. Nearly all my cases of tabes with 
mental symptoms (twelve in number) were the subjects of 



inherited insanity, and we may consider these cases as tabes 
occurring in persons potentially insane—the organic disease, 
with its complex symptoms, being sufficient to act as a 
determining factor of insanity. 


Subjective sensations of various kinds, as numbness, 
pins and needles, formication, a cold trickling feeling in the 
skin, a feeling in the soles of the feet of walking on putty, 
wool, or velvet may be complained of. In rare cases 
Hutchinson’s mask, due to affection of the fifth, occurs. 
The patient says his face feels stiff, and he feels as if it 
were covered with a cobweb. Parsesthesia of the arms, 
like the pains, affects the post axial border of the limb, the 
distribution of the (eighth) cervical and first and second 
dorsal roots. Consequently patients often complain of numb¬ 
ness and tingling in the ring or little fingers (vide figs. 1 and 
2, p. 47). The insane tabetic may put a false interpretation 
upon these abnormal subjective sensations, e.g. : Case 31 
said mice were running over her in bed at night, and she 
saw them on the pillow. Another used to get up at night 
and brush the flies out of his bed. Another (Case 27) had a 
feeling of cold water running up his back and over his head 
as far as the forehead, but not on to his face. The subjective 
sensation he insanely associated with the medicine he had 
had given to him from the London Hospital, which he 
asserted took the course in his system of this subjective 
sensation. It was of interest to learn from this patient that 
he had been warned by another patient that if he repeated 
this statement before the magistrate he would be sent away 
to the asylum. “ But he had to speak the truth ”—so 
convinced was he that the medicine was the cause of his 

Objective Sensory Disturbances. 

Forty-eight successive cases of tabes were carefully tested 
for cutaneous sensory disturbances. In forty-two cases, 
objective cutaneous sensory disturbances were found; the 
six cases in which no cutaneous disturbances were discovered 



were all in the pre-ataxic stage. Several of these pre-ataxic 
patients had had, however, subjective sensory disturbances. 
There were two other cases in the pre-ataxic stage in 
which gastric crises were associated with light tactile 
sensory disturbances of the mid-thoracic region and no 
sensory disturbance elsewhere. Trunk anaesthesia to light 
tactile impressions is the earliest and most constant sensory 
disturbance. In thirty-six cases there was anaesthesia of the 
trunk to light tactile sensation, and of these thirty-six 
twelve suffered with gastric crises. No patient suffered with 
gastric crises that did not develop sensory trunk anaesthesia. 
In most cases the affection was bilateral and symmetrical or 
nearly symmetrical, both upper and lower borders forming a 
sharp horizontal line which corresponded to the zones of 
distribution of the roots shown in the accompanying diagrams, 
Figs. 1 and 2. In this zone of anaesthesia to light tactile 
impressions, there may be a zone of analgesia or hypalgesia, 
or scattered points of blunted painful sensation. The area of 
anaesthesia or hypaesthesia of the trunk was usually more 
considerable than the analgesia or hypalgesia. The zone of 
hypaesthesia or anaesthesia is occasionally only unilateral, or it 
may be asymmetrical extending over more segments on one 
side than the other. There may be one or several segments 
anaesthetic, the most frequent being the fourth and fifth. 
Sometimes a segment above or below is hypaesthetic. In 
two cases the area supplied by a dorsal branch or branches 
of the posterior root was unaffected, while the area supplied 
by the anterior was anaesthetic. In one instance (Case 16) 
the patient was anaesthetic only over an area supplied by the 
posterior divisions of the fourth and fifth roots of the right 
side; then after an attack of severe pains in this region 
accompanied by bilious vomiting, the area supplied by the 
anterior divisions became affected and eventually a complete 
girdle of anaesthesia was found to exist. The trunk anaes¬ 
thesia is most frequently met with in the fourth and fifth 
segments ; it may extend up the chest to the third or the 
second interspace, and then the inner side of the arm also 
becomes affected. This may extend to the whole inner side 
of the arm, or only the inner side of the upper arm and fore- 



arm. In advanced cases, or cases commencing in the arms, 
there may be light tactile anaesthesia continuous with the 
thoracic anaesthesia affecting the whole inner half of the 
arm, and corresponding to the distribution of the second 
dorsal, first dorsal, eighth cervical and seventh cervical— 
that is, the whole post-axial border of the limb. It does not 
extend beyond the second intercostal space on the trunk, 

Distribution of posterior roots to the skin, after Seifier. 

because it is very seldom that the upper cervical roots which 
enter into the formation of the cervical plexus axe affected. 
In one very advanced case of tabes the whole of the skin 
distribution of the brachial plexus was anaesthetic. In this 
case (17) there was continuous anaesthesia from the fifth 
cervical to the fifth sacral, inclusive. In four cases the 



cutaneous ansesthesia of arms, trunk and legs was continuous. 
In twelve cases the arms were affected, but only three times 
did the anaesthesia extend to the radial side of the median 
line. Whilst a considerable number of the tabo-paralytics 
showed subjective sensory phenomena at some period of the 
disease, in only some cases (81, 45, 46) could objective phe¬ 
nomena be demonstrated; indeed the appearance of the 
mental symptoms not only diminished the ataxy, but the 
anaesthesia and analgesia as well. In a few cases (36-44) 
this fact could apparently be proved. One reason why more 
ataxy and more marked objective sensory disturbances are 
not met with in these tabo-paralytic cases may be that a 
great many of them are in the pre-ataxic stage, and, owing to 
the progressive brain affection, they become so demented 
that they cannot be satisfactorily tested, or they die before a 
sufficient number of root-fibres to produce such objective 
phenomena are destroyed. 

But how can we explain those cases where sensory 
disturbances have undoubtedly disappeared? Have new 
channels been opened up, or is there a dynamic change in 
the cortex cerebri concerned with the perception of tactile 
impressions ? 

In thirty-three cases the legs were analgesic or hypalgesic. 
There was usually complete insensibility to the prick of a 
needle, or the feeling only of something touching below the 
knee in all cases of tabes of the third stage, and often also 
in the later portions of the second stage. In a great many 
instances this analgesia was accompanied by light tactile 
anaesthesia. This anaesthesia was often associated with 
genital, perineal, and anal anaesthesia indicating involvement 
of the lower four sacral roots, whereas the parts below the knee 
indicate lumbar four and five and sacral one. Analgesia or 
bypalgesia of the lower extremities is sometimes limited to 
the sole of the foot or the peroneal surface of the lower part 
of the leg; it may exist independently of trunk anaesthesia 
and be the sole objective evidence of sensory disturbance. A 
patient may previously show no cutaneous disturbance and 
then anaesthesia or analgesia develops after several attacks 
of pain. 



Analgesia in tabo-paralytics is fairly common, no response 
may be elicited from the sharp pricking of a pin all over the 
body (Case 55); or the patient may exhibit a cutaneous 
sensory disturbance of two-fold origin, e.g. Case 45, where 
there existed a hemi-anaesthetic condition of the limbs on 
the left side in which there was hemianopsy, and succes¬ 
sive epileptiform seizures, leaving the other right half of 
the body free, with the exception of some analgesia below 
the knee, which shows the spinal origin of the latter and the 
cerebral origin of the former. This condition was confirmed 
by the fact that the right hemisphere weighed 100 grammes 
less than the left, also by the microscopical examination 
of the cerebral cortex. In other cases after unilateral 
seizures there was a partial hemi-analgesia and hemi-anses- 
thesia, with or without hemiparesis. 

Anaesthesia and analgesia were discovered in 42 per cent, 
of the asylum cases of tabes and tabo-paralysis; probably 
this was much less than the reality, for in a good number it 
could not be ascertained owing to the mental symptoms. 
Still some cases of ataxy, in which definite information 
showed that the patients had suffered with pronounced 
sensory disturbances and inco-ordination before the mental 
symptoms came on, not only lost the inco-ordination of 
movement, but also the sensory disturbances, after being 
admitted to the asylum. It may also be mentioned that 
the loss of painful sensation and the retention of tactile 
was, as a rule, more frequently met with, and often pos¬ 
sessed no special distribution, but affected one half or the 
whole body. 

In thirty-two cases the charts illustrating cutaneous 
disturbances in the form of anaesthesia corresponded fairly 
accurately with the distribution of definite posterior root 
areas in accordance with figs. 1 and 2, and the accompanying 
diagrams (figs. 3 and 4) were constructed from them. 

Hypercesthesia and hyperalgesia .—An area in which 
pains have been experienced, whether on the trunk or limbs, 
may be hyperaesthetic, and precede anaesthesia or analgesia ; 
it indicates the irritation prior to destruction of the root- 
fibres or their intraspinal terminals. Very frequently an 



area may be hypersesthetic above or below a complete anaes¬ 
thetic or analgesic area. A zone of hypersesthesia is therefore 
frequently met with above the third or fourth thoracic inter¬ 
space, or below the seventh or eighth. Again, there may 
be a patch of hypersesthesia situated within an anaesthetic 
area; or on one side of the trunk, or in one limb, there may 
be hyperaesthesia or hyperalgesia, while corresponding parts, 
or nearly corresponding parts, of skin on the other side 

Fig. 8. 

Diagram illustrating, approximately, the distribution of cutaneous anaes¬ 
thesia in the posterior root areas of thirty-two cases of tabes and tabo- 
paralysis. Two cases showed unequal affection of the two sides. This diagram 
shows the regions least affected are the upper cervical, lower dorsal and upper 

may he anaesthetic. Systematic microscopic examination of 
the spinal cords and their roots serves to explain these 
facts. Thus I found in pretty advanced cases of tabes a 
more complete degenerative fibre-atrophy in the lumbo¬ 
sacral and mid-dorsal regions than in the remaining seg¬ 
ments of the cord. Except in arm tabes, the degeneration 



of the roots ceased about the eighth or seventh cervical 
segments. This explains also the fact of the distribution of 
the anaesthesia shown in the diagram (figs. 3 and 4). 
Again, on one side we may have roots completely des¬ 
troyed, while corresponding roots on the other side are 
only partially destroyed or little affected. The unequal 
affection of roots will not only account for cases where 
there is asymmetrical distribution of anaesthesia and anal- 

This curve is constructed from the previous diagram. The summit of the 
first elevation corresponds with the fourth dorsal, the summit of the second 
elevation with the fifth lumbar and first sacral. It is possible that each of 
these elevations denoting tendency to degeneration of intramedullary portions 
of posterior roots may be dependent upon some morphological condition, the 
most likely being a precarious vascular supply; indeed, this is not improbable, 
for these regions of the cord depend more upon small and variant arteries for 
their blood supply than the cervical, lower dorsal, and upper lumbar regions. 

gesia, but also for hyperaesthetic zones on one side, with 
anaesthetic on the other; likewise, a widespread distribu¬ 
tion of anaesthesia and analgesia, in the midst of which 
are islands of varying size which are still sensitive to light, 
tactile sensation, or pricking of pin, may be accounted for 
by the fact that some of the posterior spinal} neurones, 
with their spinal projections and intraspinal terminals, 



are still intact. As the diagram shows, and as the charts 
in fairly advanced cases (pp. 108-113) of tabes show, there 
is usually a gap in the regional distribution of anaesthesia 
over the abdomen and thighs; these skin areas are supplied by 
the lower dorsal and upper one or two lumbar roots, and it is 
these roots which microscopic examination show to be less 
affected. Now this region is usually sensitive to pain and 
$ouch, and, indeed, may be hypersensitive. In one ease 
(14) where the skin was hypersensitive on the right 
side, deep inspiration and even movement caused severe 
pain, and the patient was thought to have pleurisy. The 
epigastric reflex was brisk on that side, whereas on the 
left side, where the skin of the abdomen was analgesic and 
anaesthetic, the epigastric reflex was absent; the cross reflex 
was, however, obtained. 

Superficial reflexes .—The superficial reflexes, as the 
previous statement indicates, were directly correlated with 
the skin sensibility, consequently the epigastric reflexes 
(excepting in very advanced cases) were generally obtained. 
The plantar reflexes were generally diminished or abolished ; 
the cremasteric and gluteal reflexes were more often present 
than the plantar, because, as we have seen, the plantar 
surface next to the mid-thoracic region is the most likely to 
have sensibility defective or abolished. 

Thermo-ancesthesia. —This was not met with nearly as 
often as affections of light tactile sensations. Regions which 
were insensitive to pricking or touching with the tip of the 
finger appreciated heat and cold; but very frequently the 
tube containing hot water could not be distinguished from 
that containing ice-cold water, and in advanced cases both 
were said to have caused a pricking or burning sensation. 
One tabo-paralytic, after once being tested with the cold 
tube, refused to touch it again, as he said it burnt him. 
Over the abdomen in the hyperaesthetic area, patients were 
generally hypersensitive to cold. Delay in response was 
frequent in all forms of sensory disturbance. This was 
generally in proportion to the intensity and extent of the 
anaesthesia. In advanced cases also, if the patient felt the 
stimulus, it was wrongly localised. Occasionally there was 


alloehiria; in one case, for example, the sensation was referred 
to the other limb, and in a few instances to a point of the 
skin above the next joint higher up in the limb. A stimulus 
which was not at first felt would subsequently provoke a 
response by repeating it a few times, thus illustrating the 
effect of summation until the neurone threshold is crossed 
by the impulse. 

Ulnar sensation of Biematsky was tested in many cases, 
and it was found that compression of the ulnar nerve at the 
elbow produced no tingling or pins and needles in the 
fingers ; but in many normal people one cannot sufficiently 
compress the nerve to produce pain. 

Insensibility to pressure of Testicles.— In some cases 
pressure of the testicles was tried, and it was found that 
pain was not produced ; but this sign, which is undoubtedly 
a useful one, was not systematically adopted. Sometimes 
impotence may be associated with this sign. 

Vibration of Tuning-fork on Bone. —Dejerine has pointed 
out that a tuning-fork placed on the bone causes no sen¬ 
sation of its vibration in tabetic patients, indicating a 
break in the path of conduction of the sensory impulse from 
bone. This sign was tried in some of the cases which later 
came under observation, and always verified in patients who 
were in the second or third stage of the disease (Case 22). 
Several cases in the pre-ataxic stage did not yield the sign, 
but I have ascertained in one case that diminished sensi¬ 
bility may exist very early, and be unequal in the two 

Visceral Disturbances. 

Bladder troubles are among the earliest and most 
constant symptoms of tabes; they are not severe, and in 
my experience the patient does not frequently seek advice 
for this reason. Comparatively few of the cases that came 
to the hospital sought relief especially for bladder troubles; 
it is only as the result of inquiry, as a rule, that the patient, 
in relating his symptoms, mentions difficulties jn starting 
micturition or holding his water. When asked if he has 
noticed any difficulty with his water, the patient will tell 
you either that he has a difficulty in starting the stream, 



requiring a strong voluntary effort on his part, or that it 
lacks force, and takes him time to empty his bladder; in 
the later stages he does not empty the bladder completely, 
consequently he frequently suffers with residual urine, and 
catheterisation is necessary. This condition indicates lack 
of power in the detrusor urinse, whereas another frequent 
condition met with, indicates loss of reflex tonus in the 
sphincter; for a cough, laughing or any cause leading to 
increased intraabdominal pressure, suffices to cause the 
escape of a little urine into the urethra, followed by the 
urgent desire to micturate. 

Bladder crises have been described, but they are rare. I 
have not met with a case. They consist of violent pains which 
occur in the lower part of the belly radiating to the urethra, 
and the inner side of the thigh. The patients have an 
urgent desire to micturate, but are unable ; they experience 
the most severe burning and cutting pains in the urethra, 
and these may be associated with lancinating pains through¬ 
out the lower extremities. These crises may last a few 
or many hours. 

In about one half of the cases which I observed there was 
a history of bladder troubles; this is much too few. The 
disparity with the results of Leimbach’s analysis of Erb’s 
patients (80 per cent, bladder disturbances) may be accounted 
for by the fact that in out-patient practice in London, where 
there are so many hospitals, many of the cases are seen only 
a few times. 

In the tabo-paralytic cases, bladder trouble, apart from 
the incontinence of dementia, was only discovered in 60 
per cent , probably again much too few, for examination of 
the spinal cords in a number of these cases showed that the 
lumbo-sacral segments of the cord were especially liable to 
the degenerative atrophy. 

Renal crises have also been described. Some of 
these cases may doubtless be due to the passage of a stone 
or gravel in a patient suffering with tabes. 

Gastric Crises .—In twenty-one patients out of sixty (36 
per cent.) gastric crises occurred, and they were not in¬ 
frequently the earliest symptom of the disease, as the attacks 



of pain and vomiting were the sole cause for which the 
patient sought relief. In one, Case 7, the patient was 
admitted for intestinal obstruction, and the surgeon was 
sent for with a view to operation. 

Eecently I have seen a case in which visceral crises were very 
severe, and tabic symptoms so ill-defined that although the patient 
was seen by several distinguished physicians, the true nature of 
the disease was not discovered, and a surgeon was called in, who 
performed an abdominal section, and found all the organs normal. 
He had absent knee-jerks at the time ; it would be interesting to 
know if he had not Argyll-Bobertson pupils and thoracic anaesthesia, 
as he undoubtedly had when I saw him later. Moreover, he said 
that before the operation his legs had given way on occasions, 
and symptoms pointing to rectal crises were recounted. I am 
informed that the reason why the operation was performed was 
the existence of pus and blood in the urine on intermittent 
occasions, plus a large movable kidney. The symptoms seemed 
also to suggest pyloric disease. 

In all cases, as previously stated, the crises were associated 
with complete or partial anaesthesia in the mid-dorsal region, 
and often with persistent subjective girdle sensation, but by 
no means every case of thoracic anaesthesia in this region 
was associated with gastric crises. This would show that 
if the crises are due to affection of afferent visceral nerves 
they are affected independently, and that the relative fre¬ 
quency and early appearance of gastric crises is due to the 
fact that they or their intraspinal terminations are under 
the same determining contributory factor to degeneration 
as the intraspinal terminals of the posterior roots supplying 
the skin of the mid-thoracic region. One intelligent patient, 
Case 3, remained in the pre-ataxic stage twenty years, the 
sole symptoms of the disease of which he was conscious 
being attacks of severe pain, “ sharp ” in character, which 
extended both vertically and transversely between the 
shoulder blades and over the whole back; as soon as the 
pain became acute, vomiting would take place and relief 
would come. He had no pains in the region of the 
epigastrium, the attacks of vomiting would last three or 
four hours. 



The attacks of vomiting may be preceded by a pain or a 
feeling of weight at the epigastrium, in one patient the 
vomiting was preceded by intense occipital headache, and a 
feeling of distension of the stomach, and this was followed 
by lightning pains through the whole body, except the face 
and the leg which was analgesic and anaesthetic. Severe 
attacks may last several days, the patient vomiting the con¬ 
tents of the stomach, whatever they may be, and the retching 
continuing with short intervals, just as in sea-sickness or 
cerebral tumour, only mucus or watery mucus frequently 
mixed with bile being voided. In several severe cases, the 
patients have occasionally vomited coffee ground material, 
or blood, due probably to rupture of congested vessels. The 
patients suffering with severe attacks are quite unable to 
retain food or even water in the stomach, and the pains may 
be so agonising that they shriek out. The tongue is dry 
and furred, the lips parched with thirst; worn out with the 
want of sleep and the distressing symptoms, it is remark¬ 
able how soon they recover as soon as the attaeks cease. 
Chemical analysis of the gastric secretion has given variable 
results, but generally the acidity is diminished. 

Occasionally the patients suffered with incomplete gastric 
crises in which there were only paroxysms of cramp-like pain 
of the stomach, or only eructations and vomiting without pain. 

One patient, Case 57, suffered for years with “ rheumatic 
pains ” and “ indigestion,” for which he was treated at several 
hospitals without relief. After three years he had delusions of 
persecution, that unseen agencies turned on electricity and blew 
up his stomach, and he was admitted to an asylum where h» 
ataxia and progressive dementia were observed. Post-mortem 
examination of the spinal cord showed the typical tabic lesion, 
and there is no doubt that he suffered with modified gastric crises. 

A few cases of gastric crises were occasionally accom¬ 
panied with frequent purgations. I did not personally meet 
with any attacks of the intestinal crises which have been 
described as occurring occasionally ; but see Case 46 of tabo- 
paralysis. They are said to be unaccompanied by pain, 
apparently suddenly and without cause, frequent watery 
evacuations of the bowels take place for days, weeks or 



months, and then as suddenly cease as they appeared. 
Bectal crises, however, are not so rare; they were met with 
in 8 per cent, of the cases, and like gastric crises were among 
the early symptoms. The patients complain of tenesmus, 
and urgent desire to stool, of severe pain in the back passage 
like the introduction of a hot iron ; sometimes this is accom¬ 
panied by tenesmus and straining, and it is said evacuations 
of blood and slime may be passed. Some of these cases may 
have been institution dysentery. Much more frequently 
the patients suffer with constipation and difficulty of reliev¬ 
ing the bowels without purgatives. Not infrequently they 
are unable to keep themselves clean. Especially is this the 
case when they have to start micturition by strong volun¬ 
tary pressure of the abdominal muscles; faeces are then apt 
to escape owing to some loss of the reflex tonic contraction 
of the sphincter ani; moreover, they cannot always tell 
when defaecation is complete. 

In 8 per cent, of the tabo-paralytic cases gastric crises 
occurred. These visceral disturbances are of great import¬ 
ance, and, in a few instances, seemed to account for the 
delusions with which the patients suffered, e.g.,'one patient 
accused the nurse of having put something chopped up in 
her milk, and of having scraped her bowels out. Case 31. 

Laryngeal Cases .—In only two cases were laryngeal 
crises met with, and these occurred early in the disease. 
This symptom was only once (Case 27) met with in the 
asylum eases, and it is relatively infrequent. The symp¬ 
toms may in some respects simulate an attack of whooping 
cough or laryngismus stridulus. One man complained of a 
sudden spasm of the glottis, with difficulty of breathing, 
which lasted a few minutes; at the time of the attack he 
suffered with a burning pain in the larynx and a feeling that 
he was going to be suffocated. By closing the mouth and 
breathing only through the nose the attacks were diminished 
in duration. The attacks are accompanied by stridulous 
inspiration and followed by short sharp coughs. The crises 
are not so frequent as visceral crises, and months or years 
may intervene. The attacks are occasionally very alarming, 
and may be accompanied by epileptiform seizures and loss 



of consciousness. These crises, together with laryngeal 
paralysis (usually adductor, sometimes one-sided, sometimes 
bilateral), are considered as evidence of affection of the 
vagus and spinal accessory rootlets. Sir William Gowers 
remarks that “ in all, if not most, of these cases of adductor 
spasm there is permanent weakness of the adductors, which, 
when considerable, constitutes a very grave complication. 
In rare cases the spasm may proceed to the pharynx, 
making swallowing impossible, and in one recorded case the 
spasm extended to the respiratory muscles, causing asphyxia 
and death.” Bronchial crises have been described, and in 
one case the onset of gastric crises was followed by dis¬ 
appearance of this symptom. 

Retardation or irregularity of the heart’s action have 
occurred in connection with gastric crises, and precordial 
pain with anginal attacks have been described (vide 
Case 27). 

Genital Organs .—Impotence may be an early or a late 
symptom. It may be preceded by satyriasis. In some cases 
impotence is associated with anaesthesia of the external 
genital organs; in some it is associated with atrophy of the 
testicles. Diminished sexual power occurred in some of the 
cases, and absolute loss of sexual power in, at least, 16 per 
cent.; this, too, may be an early or late symptom. Increased 
sexual desire is pretty frequent in the early stages of general 
paralysis and in the tabic form of the disease. 

Atrophy of the testicles is of frequent occurrence in 
general paralysis, and, generally speaking, the testicles 
lose weight out of proportion to other organs. The satyriasis 
in a tabo-paralytic may be associated with delusions of 
extraordinary sexual power; there is often marked desire, 
but no ability of performance of the sexual act. 

Sense of Position of Joints .—The sense of position of 
joints was tested in thirty cases, and in seven no appreci¬ 
able affection was shown. All of these seven were early cases, 
and the diagnosis of tabes was usually based on other evi¬ 
dence than ataxy, viz., Argyll-Robertson pupils, lancinating 
pains, optic atrophy, visceral crises, and trunk tactile 
anaesthesia. In all of these seven cases there was no appre- 



ciable disturbance in cutaneous sensibility of the limbs. In 
four very pronounced cases of Charcot’s knee-joint, there 
was no loss of sense of position discovered in the toes ; but 
one of these bad impaired cutaneous sensibility to pain and 
touch in the legs (Cases 11, 5). There was usually a dis¬ 
tinct correlation of loss of sense of position of the joints 
and the degree of ataxy, also between the disturbance of 
cutaneous sensibility and the joint sensibility. Thus, in 
one case of arm tabes, there was loss of joint sensi¬ 
bility in the arms, especially the right, in which the dis¬ 
turbance of cutaneous sensibility was most marked. In 
twenty-one out of thirty cases examined, loss of joint sen¬ 
sibility was found in the toes. In eleven the sense of 
position in the joints of the whole lower extremity was 
affected, but nine of these cases were in the third paralytic 
stage, and there was a correlated loss of sensibility to touch 
and pain, and in some cases also marked thermo-anaesthesia. 
In nine out of thirty cases the joint sensibility in the upper 
limb was affected, and in all cases accompanied by disturb¬ 
ance of cutaneous sensibility, especially of the post-axial 
border of the limb. In three very advanced and prolonged 
cases of ataxy, the joints of the whole limbs were affected; 
in the others it was only the fingers (especially the ring and 
little fingers) or the fingers and the wrist joints. In one 
case of fairly complete loss of joint sensation of the upper 
limb there was only moderate disturbance of cutaneous 
sensibility. The joint sensibility was lost in the hand on 
the right side in one case where the loss of cutaneous sensi¬ 
bility was most pronounced. The conclusion arrived at is 
that loss of sense of position in joints is a very important 
factor in the production of inco-ordination of movement; 
it is associated usually, but not necessarily, with loss or 
disturbance of cutaneous sensibility. 

The fact that the toes and fingers are affected first, then 
the ankie and wrists, and later the joints above, agrees with 
the distribution of objective sensory disturbances. No 
doubt the proto-neurons, subserving cutaneous and joint 
sensibility, are quite independent structures ; but, as a rule, 
they are simultaneously affected. I believe this sense of 



position of joints is due to a complex of sensations arising 
in alterations in tension of structures about joints, rather 
than in the alteration of contact of surfaces such as Prof. 
James assumes to be the case in judging the sense of posi¬ 
tion of limbs. It may be pointed out that no one has 
demonstrated nerve-endings in articular cartilage; there 
are, however, nerve structures in the synovial membrane 
and capsule of the joint, in the tendons, muscles, and 
fibrous structures. The most important nerve-endings are 
undoubtedly the Pacinian corpuscles, which are especially 
constructed to be influenced by alterations of tension and 
pressure in the deeper structures. In support of this argu¬ 
ment is the fact that arthropathies (Cases 5, 11) may occur 
without loss of sense of position and without ataxy, although 
I have not met with a case in which sense of position of the 
joint was lost without ataxy. 

I have met with several cases of ataxy without loss of 
sense of position of the joints, even of the toes, and 
several tabo-paralytics, who were able to give reliable 
answers, showed the early symptoms of ataxy without loss of 
joint sensation. 

Deep Reflexes .—In seven cases, not tabo-paralytics, 
nor with cerebral lesions, the knee-jerks were present on both 
sides. In three the knee-jerk was present on one side and 
absent on the other; that is to say, absent knee-jerks were 
found in less than 70 per cent, of my cases when first seen, 
but then a considerable number of the patients were in 
the pre-ataxic stage; in fact all the ten cases, except a case 
of arm tabes, were in the pre-ataxic condition, most of them 
suffering with optic atrophy or other ocular troubles; two 
came with gastric crises. In two cases the knee-jerks 
disappeared first on one side then on the other, after a series 
of attacks of lightning pains in the legs. 

The triceps jerk was not observed in the earlier cases 
which came under my observation ; but it was usually found 
absent when the knee-jerk was absent, although there might 
be no other symptoms affecting the arm. In some cases, 
however, it was present when the knee-jerk was absent; it 
undoubtedly disappears later than the knee-jerk. 



Tonus .—A diminished tonus (as tested by the Frankel 
method) was found in all but eight cases, in which the 
patients were in the pre-ataxic state. In other cases there 
was a distinct relationship between the degree of hypotonus 
and the ataxy of the limbs, and if there was a difference in 
the degree of ataxy of the two limbs it was observed that 
more marked hypotonus was present in the more ataxic 

In the asylum cases the knee-jerks were absent on both 
sides in 77 per cent., absent on one side in 16 per 
cent., present on both sides in 7 per cent. As a rule 
the hypotonus was not so marked as in the tabic cases 
met with in the hospitals and infirmaries, nor was the 
ataxy. This is possibly due to the cerebral disease with¬ 
drawing the normal inhibitory influence. With the onset of 
the mental symptoms, the inco-ordination of gait and station 
and muscular hypotonus underwent improvement, and the 
symptoms, in some cases, apparently so far disappeared that 
one was not able to prognosticate the extensive degeneration 
of the posterior columns which I found in many of them. 

If, however, the patient has advanced well into the 
second stage of tabes, the onset of the mental symptoms is 
only accompanied by a less degree of ataxy, and the 
characteristic inco-ordination in gait and. station in great 
measure persists, so that one is easily able to pick him out 
from a number of cases of general paralysis as a tabo- 
paralytic. As the brain becomes affected the ataxic gait 
often gives place to a shambling or shuffling gait, and I have 
been surprised what an extensive amount of degeneration of 
the posterior roots and posterior column of the spinal cord 
may be found in such cases. Very frequently (especially if 
the patient has had epileptiform seizures) this is combined 
with very extensive crossed pyramidal degeneration. So 
that although one was unable to obtain the knee-jerks on 
either side, yet, on the side of the fits and hemiparesis, 
Babinski’s sign was obtained, vide Case 54. 

In one case (44), however, the knee-jerk returned on 
the side upon which the fits occurred. 

Bomberg’s symptom , so frequently a constant and 



prominent symptom in ordinary tabes, may be only 
slightly obvious in asylum cases. 

25 % tabo-paralytics, slight ataxia only discoverable by careful examination. 
Romberg’s symptom absent. 

30 % ,, moderate ataxia observable in gait and station. Rom¬ 

berg’s symptom present. 

15 % ,, marked ataxia advanced second and third stage. 

30 % pre-ataxic tabo-paralytics, no ataxy discoverable; diagnosis made by 
symptoms, lightning pains, optic atrophy and absent 
knee-jerks. Very frequently subsequent examination 
of the spinal cord by careful microscopical exam¬ 
ination has demonstrated the correctness of the 

Eomberg’s symptom was very marked in only 15 per 
cent, of the cases, moderately in 26 per cent, and slightly 
in 7 per cent. 

Section III. 

Affections of the cranial nerves are less frequently met 
with ; it is not common to find the olfactory nerve affected 
in tabes, but occasionally, as my cases have shown, loss or 
imperfection of smell and the taste for flavours has 
occurred. Sometimes, as Case 10 shows, this was preceded 
by a curious and continuous odour in the nostril, like a 
drain; it is sometimes likened to rotten fish, phosphorus 
or sulphur,' and paroxysmal attacks of this perverted 
olfactory sense may precede the complete loss of smell. 
These attacks, when they occur, are of the nature of 
crises and may last hours, days or weeks; it is of import¬ 
ance to bear this in mind in connection with the subjective 
attitude of an insane tabetic patient, or a tabo-paralytic, to 
these abnormal sensations ; unable to explain their presence, 
he might put an insane interpretation on them, thinking that 
his food was poisoned, or that foul odours by unseen 
agencies were working upon him. Although loss of smell 
and the taste for flavours is uncommon in tabes, it is 
relatively frequent in tabo-paralysis and general paralysis, 
and this accords with the anatomical results found post 



mortem, for the orbital surface of the brain and the tip of 
the temporal lobe in which it is presumed the sense of 
smell and taste is located, are very generally the seat 
of extensive atrophy and thickening of the membranes. 

Sometimes the patients are said to lose sensibility of 
the mucous membrane of the nose, and no longer sneeze 
when it is irritated, or they may be subjects of paroxysmal 
attacks of sneezing and tickling of the nasal mucous 
membrane. This is due to affection of the nasal branch 
of the fifth nerve, and is rare. Other affections of 
branches of the fifth nerve are pains, anaesthesia and 
paraesthesia in various regions of its distribution. Besides 
these disturbances of sensibility, there may be various so- 
called trophic disturbances, such as a rapid falling out 
of the teeth, and absorption of the alveolus of the jaw. 
Several of the cases showed this, but in some instances 
(Cases 2, 15, 17) it may have been due to the mercury 
given in the treatment of syphilis. The sensory disturb¬ 
ances of the fifth are sometimes manifest, and sometimes 
so trifling as to be unobservable ; there does not appear to 
be any relationship of the teeth dropping out and absorp¬ 
tion of the jaw to anaesthesia of structure supplied by the 
fifth. This is in accordance with what we know of joint and 
bone diseases, which are frequently very early symptoms, 
and are in no way related to the sensory disturbances of the 
skin ; the teeth fall out without any pain being experienced. 

Other rare conditions due to affection of the trigeminus 
have been described, namely, ophthalmia neuro-paralytica 
and corneal ulcer. Both corneal ulcer and tabic ulcer of the 
mouth are analogous to the perforating ulcer of the foot. 
Again, sialorrhcea, which occasionally occurs, generally in 
paroxysmal attacks, has been attributed to affection of the 

Disturbances of taste, due to affection of the glosso¬ 
pharyngeal nerve, are very rare ; cases do occur occasionally 
in the form known as medullary tabes (see Case 62). 

Auditory nerve .—The result of affection of this nerve as 
in other cases may be irritative or paralytic. Paroxysmal 
attacks of noises in the ear like rushing water, bells or 



shrill whistling sounds, or even musical sounds may occur 
(Cases 62, 24). This, no doubt, is due to the affection of the 
neurons supplying the labyrinth ; but the neurons supplying 
the semi-circular canals may also occasionally he affected, and 
give rise to symptoms like Meniere’s disease, namely, attacks 
of giddiness or loss of balance. But it is difficult to deter¬ 
mine whether this is not really due, in the absence of other 
signs of affection of the auditory nerve, to migrainous 
attacks or slight attacks of petit mat, or the giddiness of 
congestive attacks occurring in patients who are in the 
initial stage of progressive paralysis. Occasionally, as Case 
62 shows, absolute deafness may occur. 

Diseases op the Bones and Joints. 

Arthropathy and bone affections occurred relatively fre¬ 
quently in my cases of tabes. They were met with oftener 
in women than men, and not infrequently were associated 
with gastric crises (Cases 5, 17). Spontaneous dislocation or 
fracture was often the cause of the patient seeking medical 
or surgical advice. Joint affections and spontaneous frac¬ 
tures were met with not only in hospital, but also asylum 
cases. It is of considerable importance to bear this in mind, 
otherwise officials and attendants might be charged unjustly 
with neglect or ill-treatment, when in reality a very trivial 
accidental injury or no real injury, merely turning the 
patient in bed, might be followed by spontaneous dislocation 
or fracture in asylum cases of tabes or tabo-paralysis. Not 
long since I saw a fracture of the thigh in a young man 
suffering with juvenile tabo-paralysis ; the spinal disease was 
not discovered during life, but microscopical examination of 
the cord showed the characteristic lesion. It would have been 
easy to have cast blame in such a case as this, for the imme¬ 
diate cause of death was due to infective suppuration around 
the seat of fracture. Such fractures may occur apparently 
spontaneously or as a result of a very slight injury, or even a 
false step ; they are usually quite painless, and one patient 
told me she did not know her leg was broken until she saw 



the ends of the bone sticking up (Case 71). A considerable 
number of women in workhouse infirmaries lie there inca¬ 
pacitated for numbers of years with tabic joints. One of the 
earliest cases reported by Dr. Buzzard is still in the St. 
Pancras Workhouse, where she has been nearly thirty years; 
the gastric crises and lightning pains, from which at one 
time she suffered excruciating agony, have latterly almost 
ceased. The joint affection may, as in Case 5, be the sole 
symptom causing the patient any trouble ; for of course the 
physical signs, namely, the existence of the Argyll-Robertson 
pupils and absent knee-jerks, would be unknown to the 
patient, and if there were lightning pains, they would be put 
down to rheumatism. There is no doubt that, as in rheu¬ 
matoid arthritis, hard occupations involving much use of 
joints predispose to the disease. Case 5, a stonemason, in 
whom a large painless swelling of the right shoulder-joint 
was the first symptom, is an illustration, for he used this 
arm for his hammer. Again, a carpet-planner, who knelt 
all day, had an enormous painless swelling of both knee- 
joints. The poor women I met with in the infirmaries 
suffering with Charcot’s knee-joints nearly always gave a 
history of being widows who had to earn their living by 
charing and ■ scrubbing, or by using the sewing-machine. 
The two cases of tabic foot met with, were men who had 
been in the army, and subsequently worked at a forge, and 
were, therefore, standing all day at their occupation. In the 
cases which came under my notice of joint affection there 
was usually a history of a trivial injury such as a knock, 
a false step going downstairs or from the kerb, or such like. 
The swelling was not invariably painless, and it appeared to 
me sometimes difficult to differentiate some of the cases 
from rheumatoid arthritis occurring in a person suffering 
with tabes or tabo-paralysis, had not rapid effusion into the 
joint indicated a true tabic arthropathy. 

Symptoms .—A masterly description by Charcot of the 
tabic arthropathies has led to the affection being named 
after him. He pointed out that without any sufficient cause 
a joint would suddenly swell up, owing to a serous exudation 
into it and possibly into its surrounding tissues. This 



swelling is unaccompanied by either pain or fever. In the 
favourable form the swelling may disappear after a time, 
and a return to the normal condition take place, or severe 
destruction of the joint may occur accompanied by crepitus, 
wearing away of the articular surfaces and even the bone, 
causing dislocations and luxations. The knee is by far the 
most frequently affected, after this the hip, shoulder, elbow, 
wrists, more rarely the ankle, vertebral, and finger joints. 
Marie states that from 4 to 5 per cent, suffer from joint 
affections. Among my cases there were 10 per cent. 
The joints were examined in two of the cases; one was 
hardly characteristic, for a sinus existed with dead bone 
and continuous purulent discharge; the leg was amputated 
by Mr. Walsham, the capsule of the joint was greatly 
thickened and dilated, there were numerous osteophytes, 
and the cartilage was ulcerated but not entirely destroyed ; 
there was an osteo-porosis of the bones ; some nerves were 
dissected out that were proceeding to the peroneus longus 
muscle, and separated from the surrounding tissues away 
from contact with the suppurative process. A small piece 
was cut off and teased, the fibres were found (after suitable 
staining) to be undergoing an atrophic degenerative pro¬ 
cess (Case 30), but the appearances are not unlike those 
described by Marinesco after amputation ; and seeing that 
the leg was extremely wasted and the joint so disorganised 
as to be quite useless—hence the amputation—it may be 
asserted the condition was an effect of the joint disease. 
In a case of tabetic general paralysis the knee-joints 
presented an appearance in some respects resembling 
rheumatoid arthritis both during life and post mortem. The 
capsules and synovial membrane were thickened, contained 
excess of synovial fluid, and the cartilages were ulcerated 
(vide fig. 5). The patient was too demented to say whether 
it was painless or not. This was a case of very advanced 
tabes, and there was atrophy and degeneration of the peri¬ 
pheral nerves and the small nerve fasciculi of the skin. 

In advanced cases the joint surfaces with the cartilages 
may quite disappear, and the bony structure in the joint 
may be destroyed and appear as eroded away. Proceeding 



pari passu with the atrophy there may be numbers of out¬ 
growths in the capsule and synovial membrane. Chemical 
examination shows that the bones are deficient in mineral 
matter, especially phosphates. The Haversian canals are 
dilated irregularly and filled with fat. According as the 
process affects the epiphysis or the diaphysis an arthropathy 
or spontaneous fracture occurs, sometimes both (Case 71). 
Similar joint affections may occur in syringomyelia. 

Fig. 5. 

Photograph of the articular surface of the femur from a case of 
arthropathy in a typical tabo-paralytic female with all the clinical symptoms 
of the disease. Microscopic examination of the brain and spinal cord 
showed characteristic lesions. 

A peculiar malformation arises when the joints of the 
tarsus are affected ; on the back of the foot and in the middle 
of the sole there arises a hard prominence, the foot is 
flattened and shortened and the bones of the tarsus are, as it 
were, driven into one another. Crepitus is obtained on 
movement, but no pain produced. The ligaments of the 
joints may be destroyed ; several such were met with 



both in asylum and hospital cases. Tendinous tissue may 
probably undergo similar atrophic changes, for sudden pain¬ 
less rupture of a tendon which does not tend to heal may 
take place. 

Whether the bone and joint disease of tabes is dependent 
upon a definite lesion of the nervous system is still a moot 
point. Charcot believed at first that it was due to a lesion of 
the anterior horns. Other authorities attribute it to a 
disease of the peripheral nerves, especially of those supplying 
the bones, but this condition does not occur in peripheral 
neuritis. The loss of bone sensibility may, however, be an 
early sign in tabes. I recently examined a patient who 
presented very little ataxy and yet there was very distinct 
evidence of diminished bone sensibility by Egger’s test, with 
the vibrating tuning fork. [Recently Marinesco has attributed 
it to anaesthesia and absence of'reflex regulation of the blood 
supply; it may also be due to the direct action of toxins 
upon the nutrition of the bones. 

In a large number of experiments which I made many 
years ago of section of anterior and posterior roots in 
monkeys, I never met with any change in the bone with the 
exception of one case in which the posterior roots of the 
cauda equina were ligatured on the right side so as to cause 
degeneration; the animal was killed three weeks later. 
The bones of the leg on this side were so brittle that 
I could snap them with my fingers. The right femur 
was the same size as the left, when dried the right 
weighed 7'5 grams, the left 12*5 grams. The right os 
innominatum was the same size as left, when dried the right 
weighed 5*5 grams, the left 7'7 grams. The tibiae were also 
brittle, but were used for microscopical purposes. After 
softening in chromic and picric acids transverse sections 
were cut by the freezing microtome, stained with logwood 
and eosin, and mounted in Farrant’s solution. 

There was a naked eye osteo-porosis on the right side. 
The periosteum was apparently normal. Examined micro¬ 
scopically there was a marked dilatation of the Haversian 
canals, and owing to the absorption of the intervening bone, 
coalescence had taken place with the formation of irregular 



shaped channels, which contained blood-vessels surrounded 
by a reticulum of connective tissue in which were seen 
numerous osteoclasts ; these large cells were disposed usually 
at the periphery lying in little scalloped out places which 
they filled and which they apparently had caused, by absorp¬ 
tion of the osseous substance (vide photomicrograph, fig. 6). 

Bayliss and Starling have shown that stimulation of the 
lumbo-sacral posterior roots causes dilatation of the vessels 
of the lower limb; therefore vaso-dilator excitation may have 

Fig. 6. 

Photomicrograph of section of tibia softened in a mixture of picric, 
nitric, and chromic acids, stained with alum hsematoxylin and mounted in 
Farrant’s solution. 

Magnification 300 diameter. 

been set up by the ligature and caused dilatation of the 
vessels of the lower limb including those of the hones, with 
consequent absorption and diminution of the mineral matter ; 
for although, as we have seen, the bones were equal in size, 
there was a marked difference in the weight, and micro¬ 
scopically it was found that this was due to absorption of 
the osseous matter around the Haversian canals. 



Motor Disturbances. 

The cases may be classified clinically as follows, according 
to their motor disturbances : 

(1) Motor disturbance slight or not discoverable. Pre- 
ataxic condition, disease spinal:—Loss of deep reflexes on 
one side or both sides, slight hypotonus. No subjective 
motor trouble. Objective signs only discovered by expert 
examination. Other signs and symptoms lead to diagnosis. 

(2) Preataxic condition simulated, spinal combined 
with cerebral or optic disease:—In such cases the spinal 
disease may at one time have produced subjective symptoms 
and objective signs of ataxy, and the onset of the mental 
symptoms or the optic atrophy with blindness masks the 
same, or causes them to disappear partially or entirely. 
There may be loss of knee-jerks, or the knee-jerk may be 
lost on one side only, or it may return on one side after 
a series of unilateral fits. Cases 41, 44, 65 show that these 
patients have suffered with extensive degeneration of exo¬ 
genous fibres sufficient to produce fairly marked ataxy. 
Most common in asylums. 

(3) Ataxy of first stage, subjective difficulty only in the 
dark, or with eyes shut discoverable by examination, same 
as (2) without mental affection :—Loss of deep reflexes, well 
marked loss of tonus, Romberg’s symptom moderate. 
Considerable atrophy of posterior roots, half to one-third of 
fibres and their intra-spinal projections destroyed. 

(4) Ataxy of second stage,, obvious ataxic gait, subjective 
difficulty in daylight necessitating support:—Nearly com¬ 
plete atrophy of the lumbo-sacral root-fibres, considerable 
atrophy of endogenous systems of fibres, especially descend¬ 
ing comma, septo-marginal, oval area, and Phillippe’s triangle. 
Case 39. 

(5) Paralytic bed-ridden stage, frequently accompanied 
by deformity and great muscular wasting, especially of 
certain groups of muscles, which may in rare instances 
undergo degenerative atrophy. Cases 28, 31. 

The fuller consideration of the motor disturbances is 
discussed in the pathological section, chapter “ Inco¬ 
ordination and its Pathology.” 



Cerebral Symptoms. 

I have already alluded to the frequency of optic atrophy 
in the cases of tabes and tabo-paralysis which have come 
under my observation. I will now refer to other cerebral 
symptoms. Mental symptoms occurred in about 10 per 
cent, of the cases seen outside of the asylums; some few of 
these were pronounced general paralytics of the tabetic type, 
others were tabetics with symptoms indicating early organic 
affection of the brain, and the remainder were cases of tabes 
dorsalis with associated insanity. Some of the cases seen in 
the hospitals and infirmaries afterwards died in one of the 
asylums at a near or remote period from the time I saw 
them. One case in particular, J. W., attended my out¬ 
patients for several years, affected with progressive optic 
atrophy, limitation of the field of vision, and early signs and 
symptoms of cord affection. I lost sight of him for some 
years, but found him suffering with advanced general 
paralysis in Claybury Asylum, and he died there. The same 
types of tabo-paralysis were met with in the asylums, the 
only difference as a whole between the cases was what 
we would expect: in the former the cord symptoms 
predominated, in the latter the mental symptoms. It was, 
however, a well-established fact that some patients who 
had been observed outside of asylums as cases of loco¬ 
motor ataxy, after admission to the asylums, and there¬ 
fore after the development of well-pronounced mental 
symptoms, without treatment of any kind, became less 
ataxic in their movements, the gait becoming altered. As 
in general paralysis so in tabo-paralysis, the onset of cerebral 
symptoms may be sudden, and due to seizures which are 
recognised as congestive, apoplectiform, epileptiform, and 
migrainous. The seizures may lead to a disturbance of 
consciousness, or partial or complete loss of consciousness. 
Thus a patient may be suffering with discovered or undis¬ 
covered objective or subjective signs and symptoms of tabes 
dorsalis, when suddenly, or comparatively suddenly, he is 
seized with some kind of fit. There may be a temporary 
disturbance of consciousness, a sudden feeling of giddiness, 
associated with frontal headache like migraine. Generally 



such an attack is due to circulatory disturbances of the 
brain, but it is conceivable in rare cases of tabes; frequent 
migrainous attacks may be due to disturbances of the sensory 
impressions from the semi-circular canals. These attacks 
often escape observation, until one more severe necessitates 
a doctor’s advice, then the true nature of the disease may 
be discovered by the examination of the pupils and the 
condition of the knee-jerks and other signs of tabes or 
general paralysis. This will lead to further inquiries of 
the patient for such early subjective symptoms as lightning 
pains. Often, however, the patients disregard these slight 
attacks, and such cases do not come under observation until 
more serious brain symptoms develop. Some of my cases 
show that a history obtained from the wife or friends may 
give evidence of such attacks occurring years before the 
patient suffers with mental symptoms severe enough to 
cause his admission to the asylum. Epileptiform seizures 
may be the first evidence of cerebral affection, and may 
precede or succeed spinal symptoms. Cases 36, 52, 53. 

I have frequently found, by questioning the wife, that 
her husband, previous to his coming to the asylum or 
the hospital, had a fit with convulsive spasms affecting one 
side. He had recovered from this, and was comparatively 
none the worse for it. In 30 per cent, of sixty cases of tabo- 
paralysis the patient suffered with numerous epileptiform 
seizures. In 34 per cent, there was a history of one or more 
fits, but seizures did not form a prominent symptom of the 
disease. In the remaining 36 per cent, no fits were observed 
by the friends or attendants during the whole course of the 
disease. Epileptiform seizures in the case of well-marked 
tabes, where there is presumably well-marked degeneration 
of the posterior roots, had not been notably characterised by 
inco-ordination in the convulsive spasms. This is a matter 
of some interest and will be discussed later. The epilep¬ 
tiform seizures may be slight, limited to twitching of one 
side of the face or to a limb, or they may extend to the 
whole of one side of the body, or they may become bi-lateral, 
and the muscular spasm so severe and general as to cause 
opisthotonus or emprosthotonus. The convulsive seizures 



in Case 46 were extremely interesting, for this man was in 
an advanced stage of locomotor ataxy. Los£ of consciousness 
may be partial or complete, and there is a correlation 
between the severity and the extent of distribution of the 
muscular spasm and the depth of unconsciousness; as a rule, 
when the convulsions are limited to one side, the loss of 
consciousness is only partial; the pupil is usually larger on 
the opposite side to that of the seizures; the face is con¬ 
gested, the skin perspiring freely and its surface temperature 
raised from ’5 to 1*5 degrees Fahr. on the affected side. 

When extensive convulsions occur continuing for several 
days (a condition of status epilepticus ), there may be high 
fever, even hyper-pyrexia, which may cause death. Such 
severe attacks, however, are associated not infrequently with 
the onset of an acute disease such as pneumonia and dysen¬ 
tery, which kills the patient; and if the bowel has not been 
examined, and the lungs be only in the first congested stage 
of pneumonia, the patient’s death is attributed to the 
seizures; whereas really the seizures have been excited by 
the toxic condition of the blood, and have only accelerated 
death. The same applies to epilepsy. After the fits have 
ceased, the patient recovers rapidly, and his mental con¬ 
dition may even appear to have improved. This is not 
really the case; the functional disturbance of the whole 
brain caused by the congestion has passed off, and his mind 
is therefore less affected, but the result of the fits is usually 
tissue-destruction. In my opinion, the fits are often the 
expression of an increased irritability preceding decay or 
even death of the psycho-motor neurons of the cerebral 
cortex. The degeneration of the pyramidal fibres of the 
spinal cord is most abundant on that side on which the fits 
occurred, if they are unilateral; when the fits are bilateral, 
the degeneration is proportionately great on both sides. 
My observations would show that acute death of the cells is 
due in great measure to vascular inflammatory disturbances, 
but degeneration of the pyramidal fibre-systems, especially 
those fibres which come from the leg area, may occur inde¬ 
pendently of any fits, and, as I shall show later, are due to 
degenerative atrophy commencing in the collaterals and 



terminal portions of the fibres, as in idiopathic lateral 
sclerosis and anfyotrophic lateral sclerosis. In some cases 
the changes are obviously vascular and due to arterio¬ 
sclerosis affecting the small vessels; as a rule, however, 
there are not sufficient gross changes in the arteries to 
account for the wasting of the brain. In Case 45 the right 
hemisphere was particularly affected, it weighed 100 grammes 
less than the left. Although there was such tremendous 
destruction of the right hemisphere and very considerable 
destruction of the left, the dementia was comparatively 
slight; so much so that the attendants did not think that he 
could be a general paralytic. His speech, moreover, was 
but slightly affected. He suffered with left-sided hemi- 
paresis and well-marked hemi-anaesthesia and hemianopsia. 
The cause of this is discussed in Case 48, where there 
are well pronounced left sided seizures, no hemi-ansesthesia 
resulted. There was naked-eye degeneration of the pyra¬ 
midal system of fibres on the left side of the cord, as 
in Case 45 ; but it did not extend to the pyramids in the 
medulla, and there was no gross lesion of the central con¬ 
volutions or occipital lobes. As a rule, after seizures 
affecting one side, say the right, there is temporary hemi¬ 
plegia, or hemiparesis, or temporary aphasia, and there may 
be hemianaesthesia. Usually with each series of seizures 
the speech affection characteristic of general paralysis 
becomes more marked. 

Apoplectiform Seizures. — These may be manifested in 
different degrees of severity, by slight fainting fits, brief 
lapses of consciousness described by the friends as “a look 
of bewilderment,” perhaps followed by a transitory aphasia, 
word deafness, word blindness, or verbal amnesia, or the 
patient is unable to express general ideas correctly, and the 
words that he utters have no logical sequence, or may be 
even meaningless gabble. Such conditions of speech defect 
may, or may not, be accompanied by transitory hemiparesis, 
monoparesis, or facial paresis (vide Cases 54, 56). Such 
seizures may precede by months or years all other symptoms. 
Transitory defects of speech lasting a few hours, a few days, 
or even a few weeks, are particularly suggestive of two 



diseases—syphilitic endarteritis and general paralysis. As 
a history of syphilis and signs of it will in all probability be 
discovered in either case, and whereas the one is capable at 
least of partial, if not of complete recovery, and the other, 
general paralysis (a progressive degenerative disease), is 
absolutely fatal, it is of great importance in the treatment 
and prognosis to determine from which disease the patient 
is suffering. The presence of Argyll-Robertson pupils is in 
favour of general paralysis, for in syphilitic brain disease it 
is much more common to find the*pupils inactive both to 
light and accommodation. Mental symptoms characteristic 
of general paralysis may not be present. An hereditary 
history of insanity would favour general paralysis, as, too, 
any of the symptoms of tabes dorsalis (see Cases 53, 54, 56). 
Very occasionally, as in tabes, syphilitic endarteritis may 
co-exist with the primary degenerative disease. 

Mental Symptoms .—Our psychical condition, particu¬ 
larly that relating to the. feelings and emotions, oscillates 
without ceasing about a mean point of equilibrium, and the 
extent of oscillation within the limits of health is dependent 
upon individual temperament and the circumstances of 
environment. Difficult as it is to fix the normal in the 
physical organism, how much more so in the psychical ? 

Above and below the mean point of equilibrium are 
grades of pleasure and of pain, which are reflected to the 
muscles of expression, causing synergic alterations in their 
minute tensions. Every passing feeling is thus reflected, 
so “ that there is no art to find the mind’s construction in 
the face.” 

Only those who have had the opportunity of observing 
the feelings, emotions, intellect and actions of the individual 
closely, and for some considerable time, can correctly 
appreciate a change of character, of volition, of intelligence, 
and thus gauge the earliest signs of the insidious and pro¬ 
gressive mental change which usually precedes the more 
obvious and obtrusive symptoms and signs of brain degenera¬ 
tion. Long before the patient is admitted to the asylum, 
symptoms indicating a change of character may have been 
noticed by the wife, relatives, or associates in business. If 



the man is married, the wife may tell you that months or 
years before she had become aware of his being afflicted with 
insanity, she had noticed a change in his disposition. 
Previously affectionate and kind, of an equable temperament 
and happy disposition, he has become subject to fits of 
temper; or sullen, morose, depressed, and often neglectful 
of her and the children. Or she has noticed that he worries 
over the least trifle; • accustomed to act independently, 
confident in his own judgment, he loses all self-reliance, and 
worries her over the srhallest details regarding his actions. 
He may be restless and excitable, or sullen and moping, and 
he has become a man of varied moods, and unable to fix his 
attention on any subject for any time. Or the history some¬ 
times points to the patient having been filled with morbid 
suspicions, which later become fixed delusions of persecu¬ 
tion, causing him perhaps to get up in the night to look for 
burglars, and to hide his valuables. These delusions and 
fits of temper may impel him to threaten or even attempt 
suicide or homicide, and she may be afraid of her life and 
that of her children. Again, the husband who always 
brought his money home at the week end, may have 
neglected to do so, and have become extravagant, boast¬ 
ful, and addicted to drink. Other instances occur of quiet, 
sedate and staid individuals exhibiting an antithesis of 
character, giving way to amusement, gambling, immorality, 
vice and intemperance. Sometimes the prodromal period 
may be marked by flashes of genius or exceptional brilliancy 
of artistic or intellectual power. There is nearly always, 
however, a failure of concentration and steadfastness of 
purpose to carry the schemes to fruition. The wife may 
have noticed that the patient has become careless about his 
personal appearance, untidy in his dress, forgetful of his 
business or his home affairs, especially relating to events 
that have recently happened, his mind being absorbed by 
ambitious schemes which come to naught, speculation, 
gambling or betting. These prodromal signs of a disordered 
mind may precede or be associated with early or well-defined 
symptoms of cord affection. The brain would show at this 
stage only slight macroscopic change, but definite microscopic 



Not infrequently tabo-paralytics become lustful, and 
their attempts to satisfy their increased sexual desires leads 
them to adultery and immorality, which may get them into 
trouble in the police-courts, and their disease may then be 
discovered. Too often there is a history of the home being 
broken up, and the wife and children left destitute, showing 
the necessity of an early recognition of this disease. A 
condition of satyriasis is usually followed by impotence, and 
the -history related to me by several patients, but which I 
have not included in the notes of the cases, shows that 
sexual perversions may arise in consequence. Satyriasis is 
not infrequently an early symptom of tabes, and when this 
is combined with mental affection, it may be associated with 
delusions of extraordinary sexual power, which remain as 
a fixed idea even when impotence has supervened. 

The delusions may take another form; the patient 
becomes suspicious of his wife’s fidelity, and on this account 
he may become dangerous to her and others. The most 
common mental affection which brings a tabetic or tabo- 
paraiytic into the asylums is “ acute mania,” of which we 
may consider that there are four types. 

(1) Acute mania from which the patient completely 
recovers. This form is generally due to a combination of 
several of the following factors:—(a) toxins from without; 
usually alcohol ; (b) toxins from within; (c) head injury, 
business failure, mental shock, worry and anxiety owing 
to pain suffered, sleeplessness, knowledge of suffering from 
an incurable disease, onset of optic atrophy ending in 
blindness, impotence, distress and pain occasioned by 
visceral crises ; {d) inherited psychopathic temperament. 
(Cases 28, 29, 30.) 

(2) Acute mania from which the patient does not recover, 
in which the brain affection becomes chronic and associated 
with delusions, hallucinations, and illusions, accompanied 
by dementia, which, however, is usually non-progressive, 
caused by the same factors as above; but frequently there is 
a marked hereditary history of insanity in the family 
(Case 25). 

(3) Acute mania becoming sub-acute, then subsiding 



completely, associated with dementia which is non-pro¬ 
gressive ; often a great mental improvement takes place, 
leaving only traces of intellectual enfeeblement. Such cases 
are usually tabetics who either in the earlier or later stages 
of the disease have taken to drink. After admission to the 
asylum the poison no longer acts upon the nervous system, 
and the dementia which persists is proportional to the 
organic destruction of the cerebral cortex by the alcohol 
(Cases 70, 71). It is extremely difficult to decide whether or 
not these cases are tabo-paralysis, in which the disease-process 
is arrested by the removal of exciting factors. I have seen 
a few cases of absolutely certain general paralysis arrested 
in progress for years. The patients were even discharged as 
cured (sic); within a few months or less they are back at the 
infirmary to be re-certified, and sent back to an asylum, 
where they die within a short time. Presumably they have 
been unable to stand the mental stress outside the institu¬ 
tion, and should not have been discharged. 

Many instances of the almost immediate effects of mental 
shock in inducing an acute exacerbation of the disease have come 
to my notice. The cause is sometimes avoidable— e.g., a quiet 
melancholic general paralytic developed acute homicidal and 
suicidal mania the same night after hearing the fatal nature of 
his disease discussed by the physician in a ward. A patient 
who had so far recovered that his discharge from an asylum had 
been considered advisable, was told by a friend visiting him that 
he was suffering from general paralysis; this preyed upon his 
mind, and the disease-process, which was only smouldering, was 
fanned into flames, and within three months he died from the 
disease. The same applies to tabes dorsalis, the disease pro¬ 
gresses when the patient is subjected to bodily stress, or gives 
himself up to sexual excitement, drink, and debauchery. 

(4) Mania, frequently with grandiose delusions typical of 
general paralysis, accompanied by symptoms and physical 
signs of tabes (more or less defined according to the stage of 
the cord affection), associated with dementia, which, after 
the subsidence of the mania, is found to be progressive, and 
is usually accompanied by characteristic defects of speech, 
verbal and written. The acute mania from which the 



patient suffers may be partly due to alcohol, partly auto¬ 
toxic in origin. 

As in general paralysis, cases of tabo-paralysis or tabes 
may be accompanied by various degrees of mental depres¬ 
sion, with delusions of persecution. These may be cases of 
tabes with insanity, or tabo-paralysis of the melancholic 

Hallucinations are of great importance because they 
exercise a powerful influence, even more powerful than 
perceptions, on the intellect and volition of the patient. 
Many cases of so-called hallucinations are rather of the 
nature of pseudo-hallucinations or illusions, for they are 
excited by peripheral irritation. I have already referred to 
those relating to the skin and viscera in tabo-paralysis. In 
many of those cases definite lesions were found post mortem 
to account for the symptoms manifested during life. In 
cases where there has been almost complete destruction of 
the posterior roots, there have still been the lightning pains 
and visceral crises which have been insanely interpreted. 
Many of the tabetic cases of very old standing still suffer 
with the lightning pains and visceral crises. All the while 
there are any rootlets left undestroyed by the disease, pains 
may occur and radiate all through the sentient grey matter, 
each decaying fibre serving as a fulminating agent. Among 
the many cases of optic atrophy leading to partial or complete 
blindness were a number who suffered with visual hallucina¬ 
tions—viz.: Cases 59, 64, 70. Complex visual hallucinations 
are usually of human forms or of animals—rats, cats, mice, 
lions, tigers, snakes; the human forms are generally police¬ 
men, burglars, dead relatives, or people who were supposed 
enemies; and like auditory hallucinations they would tend 
to engender and aggravate delusions of persecution. It 
is remarkable that people who are quite blind should thus 
suffer from visual hallucinations, but it accords with other 
facts. Uhtoff, in a recent monograph, has recorded a case of 
tabic optic atrophy with visual hallucinations, and he refers 
to the fact that numerous cases have been recorded of blind¬ 
ness with visual hallucinations due to various causes. Some 
of my patients were not, however, absolutely blind, and the 



hallucinations may have been caused by the irritation of the 
progressive death of the fibres. One case in particular 
which, however, was a general paralytic is of very consider¬ 
able interest in this respect: the patient was admitted with 
acute mania a potu, placed in a padded room, and while there 
he was the subject of visual hallucinations. When I first 
saw him he said black devils came and perched on his nose 
and put stinking things up his nostrils and nasty things in 
his mouth. I found he had Argyll-Robertson pupils and I 
expressed the opinion that he had general paralysis as well. 
Examination of the eyes ophtbalmoscopically showed numer¬ 
ous haemorrhages around the disc, and chorio-retinitis. A 
fortnight later when I saw him, and, presumably, the effects 
of the acute alcoholism had passed off, the hallucinations 
had changed. He now said angels came and moistened his 
lips with sweet things and exhaled sweet perfumes- up his 
nostrils. He exhibited many other signs of grandiose ideas. 
The retinae were examined after death and the observations 
during life confirmed ; likewise the degeneration of the optic 
nerves was found microscopically, vide photomicrograph 
(fig. 7). It must not be supposed, however, that the 
majority of cases of visual hallucinations are due to 
peripheral irritation caused by disease of the retina or 
optic nerves; in fact they are more likely to occur from a 
morbid condition (functional or organic) of the higher 
ideation centres, presumably situated in the angular gyri. 
Uhtoff has described, and Henschen has collected, a 
number of cases of hemianopsy due to destruction of 
an occipital lobe or the radiating fibres, and in these 
cases visual hallucinations have occurred on the side upon 
which the hemianopsy was. The only case of hemianopsy 
that occurred among my cases (Case 45) did not suffer 
with hallucinations of vision; therefore, destructive soften¬ 
ing of the occipital lobe does not necessarily, even in a tabo- 
paralytic, produce this condition ; it may be presumed that 
in those cases where hallucinations occurred, there existed a 
morbid functional or organic disease of the corresponding 
ideation centre of vision, which was excited by the irritation 
of its associated diseased perceptive centre, or the peripheral 


structures (retinae and optic nerves) connected therewith f 
vide Case 26. This morbid condition is due either to 
inherent instability or general toxaemia, the combination 
of factors being sufficient to produce the hallucinations. 

The visual hallucinations were generally 'associated, like 
the auditory, with delusions of persecution. In one case 
a condition of macropsy occurred. The patient, who was a 

Fig. 7. 

Photomicrograph of a section of the optic nerve, stained by Marchi 
method. The black circles indicate bundles of fibres containing abundant 
degenerated fibres ; it will be observed that not more than 15 per cent, are 
affected, and these doubtless corresponded to the paletus of chorio retinitis 
observed during life. 

Magnification 25 diameters. 

very intelligent man, said everything appeared much larger 
than natural. Another patient, suffering with a curious com¬ 
plex of symptoms (Case 72), complained of things moving 
which were stationary. He had very sluggish re-acting pupils, 
no nystagmus, but some difficulty in fixation of the eyes. 
He also complained of inability to estimate size of objects; 
sometimes objects and persons appeared much too large, 
sometimes much too small. People coming in at the door 



of the ward appeared like babies. This failure in judgment 
of size came on usually towards the end of the day, but it 
could be sometimes produced by making him look steadily 
at a distant object. 

The occurrence of hallucinations in one sensory area is 
favoured by hallucinations in another, thus the onset of one 
set might induce the other. 

Auditory hallucinations were frequently combined with 
visual, and generally occurred in persons with an hereditary 
history of insanity; usually associated with delusions of 

Auditory hallucinations may be simple or complex ; if 
the latter, patients complain of noises in the ears like 
rushing water or a steam whistle, ringing of bells, banging 
and firing of guns; these may be followed by indistinct 
voices which become gradually more distinct; voices may 
be heard in the distance, or close to, or within the 
patient; they may relate to persons whom the patients 
have known and (from a real or imaginary cause) have 
associated with real or imaginary pains or sufferings. The 
voices heard are usually condemnatory and accuse the 
patient of immorality, vice, crime, or brutality. In females, 
obscene sexual expressions are frequently heard, or children 
crying (Cases 62, 63, 66 and 68). 

An instructive example of systematised auditory hallu¬ 
cinations is afforded by Case 25, who said that two nurses 
from the infirmary, where he was first taken, continually 
followed him, and carried on a conversation about him, 
turned on electricity and pulled his legs at night. He 
associated the lightning pains and the cramp-like spasms 
with the voices that he heard talk to him. This case is of 
exceptional interest because for years the same delusions 
and hallucinations have persisted. Like most such in¬ 
dividuals the hallucinations are worse just before going to 
sleep; they could be produced by covering his eyes, as I 
found when testing his skin sensibility. He then said he 
heard voices say “ Too bad, Hoskyns ” ; again, when he 
heard the metronome going, he heard the voice say, following 
the rhythm of the metronome, “You must have been a 



lunatic to run away from Sydney Street.” This was precisely 
the same sentence which he said he heard, and of which we 
had a note, when he heard the metronome many months 
previously. This man also had delusions of poisoning, 
which he associated with the voices. He had had visual 
hallucinations, but later they ceased to trouble him, and 
voices were not so distinct as formerly. 

Frequently auditory hallucinations occur when the in¬ 
dividual indistinctly hears the confused sound of voices at a 
distance. The patients are suspicious and morbidly inclined; 
therefore, if they see people talking in the distance and they 
do not hear what is said, by a kind of morbid association the 
hallucinatory voices return. 

Deaf people, or partially deaf people who are insane, are 
especially liable to hear voices and to be filled with morbid 
and suspicious delusions, and in the first volume of the 
■“ Archives ” I recorded the case of a deaf mute who suffered 
with auditory hallucinations; this seems almost paradoxical, 
but he had been taught lip language and the power of 
communicating his ideas; therefore, it must be presumed 
that his kinaesthetic centres were associated with his 
auditory ideation centres of words, although the ordinary 
word perceptive centre was functionless. 

Another tabo-paralytic patient, a musician, who suffered 
with lightning pains, heard not voices, but continually the 
playing of an orchestra ; he associated it with the electric 
wires and electric currents in his body ; he continually heard 
it whenever he concentrated his attention, and being a pro¬ 
fessional flute player, he whistled very accurately the melody 
he heard in his mind, and was quite surprised that I did not 
hear it also. 

A blind tabo-paralytic woman (Case 64), who was 
subject to visual hallucinations, imagined that the people 
she heard talking, came into her bed to assault her at night, 
and it was these hallucinations and delusions which brought 
her to the asylum. The existence of organic degenerations 
which occasionally, even in sane people, cause rectal and 
clitoris crises may, in insane subjects, be a source of peri¬ 
pheral excitation, and be insanely interpreted. 



Another interesting example of an hallucination giving 
rise to a systematised delusion, is that of Case 26, whose 
wife committed suicide eighteen months previous to his 
admission to the asylum. For a long time he persisted in 
the delusion that he had opened his wife’s grave, found the 
coffin empty, and that she had come to him since he has 
been in the asylum, and he had conversed with her. These 
delusions with regard to dead relations are not infrequent; 
sometimes cases occur in which the patient has hallucina¬ 
tions and delusions that relatives who are still alive are 
dead; that they have been at the funeral and seen them 
buried; it is as it were a dream which has persisted as a 
fixed idea. 

Delusions .—Delusions of persecution are common in 
tabo-paralytics; it is natural that they should put an insane 
interpretation upon their pains and sufferings, but I have 
been rather struck by the fact that this condition applies 
more to tabetic patients with associated insanity than to 
tabo-paralytics ; for grandiose delusions, exaltation, bien-etre , 
supervene very frequently in tabo-paralysis. As the mind 
becomes affected, and especially after an attack of mania, 
leaves the patients demented, they cease to complain of 
pains, and the cord symptoms both subjective as well as 
objective, are less obvious, and may even almost disappear. 
The subjective symptoms disappear with the progressive 
destruction of the seat of consciousness, and this may 
account for the well-known fact that paralytics do not suffer 
much pain from bodily injury or disease, and hardly ever 
complain ; so that a patient may have a very severe and 
painful affection of the internal organs without manifesting 
any subjective or even objective symptoms during life. 
In such a painful disease as dysentery, with its attendant 
gripes and tenesmus, I have been struck with the fact that 
demented patients seldom complain or evince signs of pain. 

In 28 per cent, of the sixty asylum cases of tabes, the 
patients were affected with delusions of persecution, poison¬ 
ing, electricity, &c. In three-fourths of such patients, there 
were either auditory or visual hallucinations, often the two 
combined; and all of them, with one exception, had an 



hereditary history of insanity. Nearly all the cases of 
hallucinations had an hereditary neuropathic or psycho¬ 
pathic history. The grandiose cases were apparently much 
less subject to hallucinations of vision and hearing, and an 
hereditary history of insanity was comparatively less frequent. 
Grandiose delusions alternate occasionally with those of 
persecution ; mania gives place to melancholia, and restless 
excitement to stupor. The grandiose delusions do not seem 
to be so persistent as those of persecution, and it was 
frequently noted in the sixty cases collected that they passed 
off after the patient had remained in the asylum a little 
w 7 bile, and the acute delirium had subsided. It seemed that 
some were partly due to the effects of acute auto-intoxica- 

The delusions of persecution associated with electricity 
in the body, the poisoning of food, twisting of the bowels, 
withdrawal of the semen (impotence), bad smells and tastes, 
frequently associated with hallucinations of sight and hear¬ 
ing, have, I conclude, an organic basis in the tabo-paralytic, 
and persist generally throughout the illness, although 
different false interpretations may be put upon the abnormal 
sensory stimuli. The grandiose delusions were often simply 
confused, incoherent, and grotesque exaggerations referring 
to the patient’s possessions or ambitions. Thus in E. C. R. 
and his wife conjugal paralysis (Case 69), the prevailing delu¬ 
sion in both was the ownership of all the furniture of the 
asylum ; the man was a furniture dealer. Another man was 
a cutter in an army tailoring establishment; one of his 
delusions was that he was a colonel in the Lancers ; another 
that he possessed diamonds; but the fact that he was a 
Polish Jew, who had for a long time been in South Africa, 
makes it possible that he was once in the illicit diamond 


Progressive dementia is the most constant symptom in 
general paralysis ; it also exists in all cases of tabo-paralysis, 
but as a rule, according to my experience, death takes place 



before there is advanced dementia more frequently in cases 
of tabo-paralysis, than in ordinary cases of general paralysis. 
This is but to be expected, since the degenerative process 
which has affected the central nervous system has either 
been in progress in the spinal cord some considerable time, 
or when it attacks both the spinal cord and the brain simul¬ 
taneously, death from one of the many complications arises 
sooner; and the fact that both cord and brain are affected 
indicates a more widespread process of decay. A man who 
has suffered with tabes for five or six years, and is then 
attacked with brain symptoms, as Case 46, is in a lower 
state of vitality than a man who starts with brain symp¬ 
toms ; but if we consider that the disease is a single morbid 
entity, and began with the cord symptoms, then the duration 
is longer. Be that as it may, it is a fact that, in cases with 
tabes dorsalis, at the autopsy one finds as a rule less brain 
wasting than in an ordinary case of general paralysis. The 
majority of the cases recorded exhibited either a slight or 
only a moderate degree of brain wasting, and we know that 
the dementia, generally speaking, is proportional to the 
extent of the brain atrophy. 

The following cases, 45 and 48, were attended by left¬ 
sided seizures during life, the epileptiform fits being the. 
immediate cause of death ; these patients did not exhibit 
marked dementia, and at the autopsy one found very great 
wasting of the right hemisphere. This was particularly so 
in Case 45. Another case, 54, with right-sided seizures 
exhibited marked progressive dementia, and at the autopsy 
the left hemisphere was found markedly wasted, and weighing 
much less than the right. Seeing that the speech centres are 
situated in the left hemisphere in right-handed persons, it may 
be considered that the mental state did not really indicate a 
more marked dementia, but a greater difficulty in expression 
of ideas and the ideation of words. Although both hemispheres 
are simultaneously used in all mental processes, and it is not 
suggested that the left hemisphere is used independently of the 
right, even in speech, yet it is through the left hemisphere and 
its centres connected with verbal and written speech that the 
brain as a whole carries on all abstract processes of thought; 



therefore, it must be allowed that one could ideate words and 
think in the abstract to some extent without the action of 
the right hemisphere, but without the left hemisphere this 
would be impossible. 

The most dementia occurs when both hemispheres are 
wasted. In some acute cases where there has not been time 
for the products of decay to have been removed and absorbed, 
there may be extensive dementia without very great wasting, 
but examination of the tissue microscopically shows an acute 
cell destruction, generally associated with marked vascular 
congestion and cell-proliferation in the peri-vascular lym¬ 
phatics. It was remarkable in some cases, especially Case 
31, how cord and brain symptoms seemed to alternate, as if, 
while the process was destroying the structures in the cord, 
in the brain it ceased, or was in abeyance. 

Note .—The morbid anatomy and pathology will be 
described after the cases. 





A summary of the clinical symptoms of cases of tabes 
which have presented some unusual clinical phenomena, or 
are adapted for explanation of some essential feature of the 

Case 1. —Optic atrophy at 19. Prcataxic condition for twenty- 
eight years , probably due to congenital syphilis , although no 
history was obtainable. —(Bethnal Green Infirmary.) 

J. E., aged 47, lost his sight between 19 and 20 ; he accounts 
for it by a blow on the head when 11 months old. Twenty-five 
years ago he attended St. Bartholomew’s Hospital, under the care 
of Dr. Hensley, who then said that he had locomotor ataxy. He 
is very positive in saying that he had nothing to do with women 
before he went blind. He says that he does not see how it can be 
locomotor ataxy, for up to a few weeks ago he was able to walk 
eight or ten miles a day. Four years ago he was treated in the 
London Hospital for severe gastric crises. He has now gastric 
attacks occasionally, which last two or three days. He has a 
feeling of a tight cord round the waist, cutting pains in the legs, 
and a somewhat ataxic gait. Cutaneous sensation is nowhere 
lost in the legs, but light tactile sensibility is lost over the thorax 
and back between the fourth and tenth segments inclusive. In 
this region also there is some hypalgesia and considerable delay. 
The joint sensation is good everywhere except in the great toes. 
Knee-jerks and triceps jerks lost, moderate hypotonus in the legs. 
The pupils had had atropine put into them, they could not 
therefore be examined. Optic atrophy of old standing. 

Case 2.— Case of hereditary syphilis in a child , whose father died 
of general paralysis. At the age of 9 paroxysmal attacks of 
severe pain in the abdomen associated with vomiting and 
sometimes diarrhoea . A previous history of ten fits. Admitted 
to Charing Cross • Hospital , subsequently to Darenth. Absent 
knee-jerks , optic atrophy , chorio-retinitis , pupils dilated , equal , 
inactive to light and accommodation; trunk , light tactile 
anaesthesia and dislocation of hip. 

P. C., aged 9, admitted to Charing Cross Hospital, May 21, 
1899, for attacks of vomiting and pain in the abdomen. 



Family history .—Father died at Banstead of general paralysis 
of the insane. It may here be remarked that the notes of his 
case did not refer to syphilis or any signs thereof on his body, but 
his offspring indicates that he suffered with this disease. Mother 
had two children born dead and one miscarriage. The patient 
began to have the attacks of pain and vomiting at the age of 7, 
and they became as frequent as once a week. The child also 
complained of pains in the bones and joints, and two years ago 
she had swelling of the dorsal surface of both feet. 

Condition on admission .—She is well nourished, and presents 
signs of hereditary syphilis in well-marked rhagades on the lower 
lip and at the angles. Complete loss of knee jerks, but no other 
physical signs are mentioned in the notes, although they show 
that all the organs were carefully examined. 

At Darenth in June, 1899,1 saw her. She had then recovered 
from an abscess of the jaw and a pelvic abscess which had been 
opened ; the attacks of vomiting still persisted, attended with 
radiating pains. Knee-jerks absent. Pupils dilated, unequal, 
inactive to light and accommodation. 

December, 1901.—The following notes as to her condition 
were kindly forwarded to me by Dr. Beresford : Pupils dilated, 
equal, inactive to light and accommodation. Very defective 
vision of left eye, ophthalmoscopic examination shows chorio¬ 
retinitis and white atrophy of the disc. Optic atrophy of the 
right eye and chorio-retinitis. Knee-jerks absent both sides, 
triceps jerk present, superficial reflexes absent. Anaesthesia of 
chest to light tactile sensations from the third rib to the upper 
border of the sixth rib, extending lower in the left axilla than in 
the right. The rest of the body and limbs are normal to touch 
and pain. Very little loss of sense of position of joints. She has 
slight incoordination, and sways rather when standing with the 
eyes shut, but she has a dislocation of the hip. She still suffers 
with gastric crises, attended by severe pain. Her mental 
condition as a rule is normal, sometimes bites her tongue, and 
passes her urine and motions under her. At other times she 
has control over the sphincters, and responds to the calls of 
nature. She has thickening of the left femur in upper half, and 
a dorsal dislocation of the head of the right femur. There are no 
teeth in the lower jaw, and the alveolus is absorbed just like an 
old woman’s jaw. The alveolus of the right half of the upper 
jaw is gone, and all the teeth, except one central incisor. Left 
side of the upper jaw one upper molar, first and second bicuspids, 
lateral and central incisor are still left. (?) Result of mercurial 
treatment or atrophic bone lesion. 


Case 3.— Preataxy. Gastric crises of twenty years' duration still 
severe in character . Impotent five years . 

C. E. M.‘, sailor all his life up till the last eight years, since 
then a publican : later on an Admiralty messenger. Married. 

Family history. —No direct neuropathic history. One of a 
family of seventeen children, five of whom are now alive. Patient 
does not know whether his mother ever had any miscarriages. 
His eldest brother died at the age of 50, from some brain trouble. 

In 1878 he contracted syphilis (hard sore, scar still remains). 
In 1881 he was engaged stowing away provisions in the ship’s 
hold, and strained himself. He had an inflammatory swelling in 
the groin which was lanced on two or three occasions, and from 
which he was not entirely free for three months. Patient not a 
free drinker. 

Present illness. —Patient.dates the onset of the present illness 
after the occurrence of the buboe in 1881. The first thing that 
occurred was a pain in the back, sharp in character, which 
extended both transversely and vertically all over the back: at 
first the pains only lasted about a day. As soon as they became 
acute vomiting commenced, and relieved them. There were no 
pains in the region of the epigastrium. At first these only came 
once in six months, but later became more frequent and more 
severe. In 1895 patient married ; at this time the attacks of 
pain occurred about once in every three months and would last 
three to four days. The attacks of vomiting would last two to 
three hours, but now did not relieve the pains. He now began to 
notice that on washing his face, he had a tendency to fall down, 
and began to have very sharp lancinating pains shooting down his 
legs. After marriage his sexual powers declined. The desire for 
intercourse was still present, but the erection would die away with¬ 
out full performance of the sexual act; in fact (since 1895) he 
has never been able to completely perform the act. For the 
last three to four years he has had a sensation of wool under the 
soles of his feet. Also has had occasional attacks of difficulty in 
passing his water, not amounting to actual retention. The bowels 
are regular. For the last five or six years he has had a sense of 
constriction round his body. This feeling is synchronous with the 
pain. He has never suffered with diplopia. He has noticed no 
change in his gait nor powers of walking. His principal trouble 
is the increase in the frequency and severity of the pains, which 
have become very bad. They come on now every two or three 
weeks and last for a few days or weeks. Associated with the pain 
is intense sickness, which occurs whether there is food in the 



stomach or not. This vomiting persisted on the last occasions for 
twenty-four and fifty hours respectively, the attacks coming on 
at an interval of about half an hour. It is extraordinary how soon 
the patient recovers and is able to take ordinary food after such 
severe attacks; this then, resembles sea-sickness. Patient has 
lost flesh considerably during the last few years, but does not feel 
weaker except after one of his bouts of sickness. 

Present condition , January 19, 1900.— Nervous : (a) Motion— 
Hand grip unimpaired. Muscular power in legs good ; the muscles 
show no signs of atrophy, but are flabby. No incoordination of 
movement. Slight hypotonus of muscles in right leg. ( b ) Cuta¬ 
neous sensation was charted and showed hyperaesthesia over the 
thorax, but no definite anaesthesia. Muscular sense unimpaired. 
Reflexes —Superficial :—Plantar reflex well marked on the left 
side. Plantar reflex absent on the right side. Cremasteric — 
Present on the right side, but very sluggish; brisker on the left 
side, but less marked than normal. Epigastric —Brisk on both 
sides. Deep Reflexes —Knee-jerks absent on both sides. Gait — 
Normal. Stands pretty well on one leg. Stands erect with 
eyes shut. Ocular —Pupils slightly contracted and unequal, left 
smaller than right. No reaction to light, but to accommodation. 
Gastric crises still continue and he is now suffering from diplopia 
owing to paralysis of the left external rectus. 

Case 4.— Transitory paralysis of left external rectus , gastric crises , 
preataxic condition , knee-jerks present both sides , cutaneous 
thoracic ancesthesia unequal on two sides . Brother died in 
asylum of general paralysis. — (St. Pancras Infirmary , August, 

J. M., aged 45, occupation pavior and mason, work hard; 
married, has had sixteen children, six of whom are alive, one 
miscarried, and three born dead in succession ; denies syphilis. 

Family history .—Brother died in Colney Hatch two years ago 
of general paralysis, aged 36. He lived a very rackety life, and 
was the subject of syphilis, undoubted. 

History of illness .—Four years ago he had double vision and 
paralysis of the left external rectus, gastric crises. He has no 
ataxy, no pains in the limbs, no paraesthesia, no difficulty of 
walking in the dark. The knee-jerks are present on both sides 
upon reinforcement, triceps and wrist tap both obtained, no loss 
of sense of position, joint sensation and localisation perfect. The 
only symptoms are double vision, slight nystagmus to the left. 



Argyll-Robertson pupils and the gastric crises previously men¬ 
tioned, which were extremely severe, causing him to shout out, 
and were only relieved by morphia. He is sick with no food in his 
stomach, and during these attacks he has a deep epigastric pain, 
and pain under the right shoulder. The vomit is very frequently 
bilious. There is no enlargement of the liver or gall bladder. 
There is some dilatation of the stomach. There is light tactile 
anaesthesia over the fourth, fifth, and sixth segments on the right 
side, and the fourth segment on the left side, which is of interest, 
seeing that it is on the right side that he feels the pain when the 
crises occur. He has no analgesia or thermal anaesthesia. His 
answers are reliable. 

November 14, 1901.—Patient is very depressed, still suffers 
with gastric crises. Complains of shooting pains down the spine. 
He has diplopia and paralysis of the left external rectus. A. R. 
pupils equal 3*5 ram. He complains also of pains across forehead 
between the eyes (probably sympathetic associated). Knee-jerks 
present right side ; present on reinforcement on the left. Hypo- 
tonus more marked on the left than right. Retention of urine. 
Cutaneous disturbance unchanged. 

Case 5.— Tabo-arthropathy , preataxic condition for twenty years . 

J. L., aged 63. At the age of 43 he came to Charing Cross 
Hospital suffering with lightning pains, Argyll-Robertson pupils, 
absent knee-jerks, and a large swelling of the right shoulder 
joint, preceded by pain, and greatly distended with fluid. 
It rendered him unable to follow his occupation of stone¬ 
mason. He weilds a 4-lb. hammer with the right hand 
to strike a chisel held in his left hand ; both the metacarpo- 
phanlangeal and the phanlangeal joints (especially of the 
thumbs), also the left elbow and wrists, present nodular 
deformities, like that of rheumatoid arthritis. The joints of 
the lower limbs exhibit little or no deformity. He admits 
having had a chancre when he was 22 years of age. 

December, 1901.—The patient has been re-admitted to the 
hospital. He is still in the preataxic stage, knee-jerks and triceps 
jerks are absent, lightning pains are now present and very severe, 
pupils unequal, right four, left three-and-a-half mm., inactive to 
light, but react somewhat sluggishly to accommodation. There is 
no ataxy in the gait; Romberg symptom is not present; there is 
no loss of sense of position in the joints, or any marked inco¬ 
ordination of the lower limbs ; owing to joint deformities it is 
impossible to say whether there is any in the upper limb or not. 



There is no trunk anaesthesia, and, with the exception of a little 
confusion of the prick of a pin with the touch of a finger in a few 
spots in the lower part of the peroneal borders of the limbs, I 
could discover no defect of sensation anywhere ; he has never had 
any trouble with his bladder, or any other visceral symptom 
beyond the attacks of vomiting mentioned. The right shoulder 
joint was tapped some time ago, the swelling has therefore 
gone down. {Skiagrams of the various joints have been made ; 
there appears to be absorption of the head of the humerus and 
ankylosis. Considering the deformities of the hands there are 
very few osteophytes, and most of the swelling must be due to 
the capsules and the synovial membrane round the joints. The 
left elbow joint does, however, show a considerable amount of 
osteophytic growth. The joint disease in the upper limbs has 
produced a fair amount of muscular atrophy. 

This case is of interest in several ways, firstly, because the 
diseased condition of the joints of the upper limbs was probably 
connected with his occupation of a mason, which he had followed 
for thirty years ; secondly, the absence of bladder trouble and the 
long period during which the patient remained in the pre-ataxic 
stage. The sense of position in the joints, in spite of the 
deformities, remained unchanged. 

Case 6.— Woman. Advanced tabes , well-marked signs and history 
of syphilis. Brother died in asylum of general paralysis. 
— (Bethnal Green Infirmary.) 

E. C., aged 48, married. One child born dead eighteen months 
after marriage, no pregnancies since, papery scars all over body, 
undoubtedly syphilitic, occupation sewing machinist. Brother 
died in an asylum of general paralysis, aged 46. Her illness com¬ 
menced with lightning pains, numbness in the hands, followed by 

Present state .—Marked ataxy, Romberg symptom, loss of 
joint sensation in the feet, legs, and hands. Deep reflexes lost, 
and loss of sense of position in both upper and lower limbs. 
Superficial reflexes, plantars absent, epigastric present. Pupils 
unequal, left irregular 3| mm., right 5 mm. inactive to light and 
accommodation, marked hypotonus of legs. 

Sensation .—Thoracic anaesthesia in area of distribution of 
seventh and eighth cervical upper dorsal, third, fourth, and 
fifth lumbar, first sacral, and hyperaesthesia in areas between. 
Imperfect localisation over the lower part of abdomen and 



upper part of legs. Pricking with a pin is described as a touch 
all over the body. 

Case 7.— Case of gastric crises admitted for acute intestinal obstruc¬ 
tion. Operation contemplated; contracted pupils with inaction 
to light attracted attention and averted operation . 

W. C. Labourer. Single. Admitted Charing Cross Hospital. 
August 17, 1900, for violent pains in the abdomen. 

Family history. —Nothing of interest. 

Personal history. —Influenza and pneumonia three years ago. 
Syphilis contracted fourteen years ago (hard chancre, secondary 
eruption, falling out of hair). Treatment (?) 

Physical signs. —Has been troubled with his bladder for the 
last eight weeks. Has great difficulty in passing his water, and 
intense pain when he endeavours to micturate. Sometimes has 
difficulty in passing his motions. Has been a free drinker for the 
,last two years. Patient first experienced difficulty in walking 
two weeks before admission. He has had peculiar sensations in 
the abdomen for the last four or five weeks, such as sense of 
constriction, like a tight cord, and at times, sensations of 
cramp. Shooting pains have occurred in the right leg only. Has 
noticed failure of sight for two years, and cannot now see to read. 

Present illness. —On Friday morning, August 17, he woke with 
violent pain in the abdomen; this became so bad that he came to 
the hospital. When seen he was breathing very rapidly, and 
appeared to be in great distress. Pulse quite good, and he had 
not been sick. On examination of the abdomen, the lower part 
of it was found to be slightly distended, but everywhere tym¬ 
panitic, except in the supra-pubic region. Abdominal move¬ 
ments good. On palpation nothing definite was felt. There did 
not appear to be any tenderness, and the abdominal wall was 
equally soft all over. What swelling there was, was most marked 
over the left inguinal region. At first there was distinct gurgling 
all over the belly ; palpation seemed to aggravate the pain. With 
a diagnosis of probable acute intestinal obstruction (volvulus ?) he 
was admitted. His rectum was then examined, but nothing 
abnormal was found. As the pain increased, and the patient was 
becoming slightly delirious, J grain of morphia was given and an 
enema ordered. When the latter was administered, the patient 
was sick; after this he quieted down, breathing quite quietly and 
sleeping. At five a.m. he was seen in this condition, and a 
catheter passed without attracting his attention, and 14 ozs. of 
urine drawn off. Specific gravity 1-005, acid, and contained a 



faint trace of albumen. At seven he vomited, and continued to 
do so at intervals throughout the day, the vomit being brownish 
acid ; no blood or stercoraceous smell. The pain returned as the 
effects of the morphia passed off. Mr. Boyd saw patient at 
ten a.m., and as the pulse was good (84), he decided to wait and 
watch for further indications. At eight p.m. the patient was 
complaining of pain higher up in the abdomen, and of pain in the 
back and loins, as though someone was pinching him in. This, 
-combined with the fact that the pupils did not dilate during the 
paroxysms of pain, led at once to a suspicion of locomotor ataxy, 
and on examination typical symptoms were found. While patient 
has been in hospital, he has on several occasions been quite 
delirious, and has got out of bed and walked aimlessly about the 
ward; It was found that these attacks were associated in some 
peculiar manner with a full bladder. In these delirious attacks 
he suffered with visual and auditory hallucinations. He stated 
that he heard numbers of men continually tramping up the stairs 
in the night, and that they came and marched through the ward 
like an army. 

Examination of present condition . — Well-built and well- 
nourished man. Motor power. —There is no wasting of muscles, 
and the power in the legs and arms is good. Hypotonus of 
muscles is well marked. When patient is lying on his back the 
leg can be flexed to a right angle with his body when the knee is 
extended. Sensation. —The buccal mucus membrane on the right 
side, also the tongue (right half) were anaesthetic and analgesic, 
as well as the whole cutaneous surface of the right half of the 
body; but the cornea was very sensitive to the slightest touch. 
There is slight incoordination of the legs and arms. Eyes .—Argyll- 
Robertson pupils. There is no paralysis of the external ocular 
muscles. There is great diminution in the field of colour vision 
on both sides, and optic atrophy. Muscular sense is much 
impaired on the right side of the body. Gait ataxic; Rom¬ 
berg’s phenomenon well marked. Reflexes. —Knee-jerks absent 
on both sides. Plantar, cremasteric, and epigastric are con¬ 
siderably diminished. 

Case 8.— Case of (probable arsenical) neuritis from beer drinking — 
attacks of vomiting—pains in legs and absent knee jerks .— 
Thought to be tabic with crises , but pupils normal. 

W. W., aged 70-years, occupation boiler maker, married, 
five children, one dead. He has worked in the North of England, 
having been sent there. 



Previous history .—Has had jaundice three times, accompanied 
by retching and attacks of sickness. He was brought into 
Poplar Infirmary suffering with vomiting, sneezing, and itching of 
the eyes. He was unable to walk or stand, had burning pains in 
the legs and in the soles of his feet and cramp. 

Since admission .—He has had no attack of sickness for four 
months, and from the first there has been a steady improvement. 
At the present time there is great tenderness in the calves of his 
legs, and the knee jerks are absent. He has had delirium 
tremens, and has drunk large quantities of beer. There is 
marked pigmentation of the legs. The 'pupils react to light and 

Case 9.— Preataxic condition . Optic atrophy , interesting syphi¬ 
litic history . 

G. P., aged 48. Occupation, ship’s steward, hard chancre 
twenty-five years ago, followed by sores on the body and rash. 
Treated three months. Married at the time, but away from 
his wife on a voyage, and he remained away years. He 
was infected with syphilis in 1876, and returned home in 1878. 
His wife, who had had one child in 1873, now suffered with three 
successive miscarriages, one in 1878 and two in 1879. In 1880 
she became pregnant, child born dead, and again in 1881, when 
she began to give birth to healthy children, so that she has now 
five healthy children living. This is best shown in the subjoined 

First child 1873, male, alive and well. 

Husband, in 1874, went for a voyage lasting three-and-a-half 
years ; in 1876 was infected with syphilis ; returned home in 

During 1878 and 1879 the wife had three miscarriages. 

Child born dead 1880. 

Second child, 1881, male, alive and well. 

Third ,, male, alive and well. 

Fourth „ ,, ,, 

Fifth ,, „ 

There is no history of nervous disease or insanity in his 
family; he has never been a heavy drinker, but has suffered with 
malaria, yellow fever and cholera. 

Present illness .—Ten years ago (that is, sixteen years after 
infection) he noticed he saw double for about ten or eleven days. 
Twelve months ago sight began to fail in the right eye, of which 
he has now completely lost the sight ; there is also dimness of 
vision in the left eye. He has complained of no shooting pains, 


numbness, formication, girdle sensation, or inability to walk in the 
dark, but for some time he has noticed a frequent desire to make 
water and occasional incontinence. 

Physical signs .—Optic atrophy both sides, pupils unequal, 
somewhat irregular, right measures 5£, left, 4f mms., inactive 
to light, active on convergence ; limitation of field of vision on left 
side, but recognises colours. Knee-jerks right, brisk left, present; 
bo parsesthesia, no Bomberg symptom; no ataxic gait; no 
anesthesia or analgesia anywhere. This case is of interest 
because, probably, the wife was not infected, for in 1881 she gave 
birth to a healthy child. It is quite possible that the three mis¬ 
carriages in 1878 and 1879, and the dead child in 1880, were 
due to spermatic infection and defect of the male germinal plasm. 

Case 10.— Squint, optic atrophy . Loss of smell and taste of 
flavours ; very mild gastric attacks , only very slight sensory 
cutaneous disturbance of thorax , preataxic condition . Knee 
jerk present on one side , absent on the other. 

C. F., aged 57. Occupation, barman, billiard marker, coach¬ 
man, and finally shoe finisher for thirty-four years. Married at 
twenty, nine children in thirteen years, four alive, two died since 
wife died thirteen years after marriage. Ptosis and continual 
squint in right eye was the first symptom, occurring five years ago. 
Twelve months before this he had “ a sore in the pipe,” which 
healed up as the discharge was cured; the discharge only was 
treated. Fraenum absent, two brown pigmentary patches symmet¬ 
rically placed on each leg. Glands in right groin shotty. Went 
to Moorfields for seven weeks, and the medicine they gave cured 
the squint, but left the pupil large. Three years later went again 
owing to sight becoming misty in both eyes, and that became 
worse and worse (not a great smoker). Dull pain across fore¬ 
head ; difficulty with his work two months before Christmas, 
1898. Numbness over the breast, armpits, and flanks ; he knew 
that there was impaired sensation there. Nothing on inner side 
of arm. He had cramp in the calves, but no numbness in the 
feet. For the last few months he has experienced difficulty in 
passing his water; has been constipated for several years. No 
gastric crises. Complained of pain over pit of stomach for two 
years, with flatulent distension, but no sickness. The least little 
jerk hurt him, and he was very tender over the epigastrium. 
Experienced no difficulty in walking. Loss of smell since para¬ 
lysis of right eye, but has a very disagreeable sensation of smell 



like a drain. He can taste mustard, sugar, acid, and salt, but no 
flavours; therefore only olfactory affected. He cannot smell or 
taste peppermint or aniseed (tested). He can smell ammonia. 
Knee-jerk present left side, but absent right side. Hypotonus 
both sides, angle nearly 90 degrees with body. No loss of sense 
of position in legs or toes, a little loss in hands. No loss of sexual 
power. Used to lurch to the right when he had paralysis of the 
right eye. Superficial reflexes all present in trunk and lower 
limbs. Cutaneous sensibility, anaesthesia to light tactile im¬ 
pressions in the fourth and fifth thoracic segments left side, 
and over a region corresponding to the sacral roots. No thermo¬ 
anaesthesia either to heat or cold. Optic atrophy in both eyes, 
marked curving of vessels which are of normal size. 

Case 11.— Charcot's joint , both knees , in a carpet planner , who 
knelt all day , slight cutaneous thermo-ancesthesia , otherwise 
very slight symptoms of tabes . 

W. J. S., aged 56. Occupation carpet planner for twenty years 
(before that a carpenter) involving kneeling twelve hours a day. 
Married at 21, child born healthy twelve months after, alive, aged 
32 ; twelve months later another child was bom, and twelve 
months after that a girl, no addition since. No miscarriages. 
Always suffered with rheumatics, in fact for thirty years. When 
18-19 had gonorrhoea which lasted three months. Patient, how¬ 
ever, denies syphilis. Father lived to 86 years, mother to 84. No 
neuropathic history. Pains in legs, came on severe ten months 
ago. A few months later an enormous spontaneous painless 
swelling in the left knee: he was able to kneel on the right 
knee, then it became similarly affected. No pain in the legs now. 
No girdle sensation, difficulty with water, bowel symptoms, or 
gastric crises. Does not complain of unsteadiness in walking and 
could walk in the dark very well. Pupils, no reaction to light or 
pain, react to accommodation. Field of vision normal. The glands 
in the groin are enlarged, the right testicle is twice as large as the 
left, otherwise no suspicion of syphilitic residua. He has com¬ 
plained of pains in the legs as well as the arms, but the arms 
were affected later. There is not very marked alteration of 
sensory perception, but there is delay in appreciating light tactile 
sensations and slight imperfect localisation of the same, in region 
corresponding with the distribution of seventh and eighth cervical, 
upper six dorsal and the lumbo-sacral roots. There is no loss of 
sense of position in the hands and the patient feels quite well any 



movement of the toes, and he knows exactly what is being done 
when they are moved. Knee-jerks cannot be tested, nor hypotonus. 
It was remarkable that the patient's power of appreciating the 
painful sensation of the prick of a pin in the legs seemed to 
increase as the experiments were continued, as if increased con- 
ductibility had occurred. In the limbs below the knees where 
painful pricking was confounded with touch sensation, one ob¬ 
served confusion of heat and cold ; generally speaking a hot test 
tube was thought to be cold. When tested in the abdomen, 
thorax or face, he made no mistakes. There are large corns over 
ball of little or big toes in both feet which look as if they 
would soon become perforating ulcers. The Charcot knee joints 
are very characteristic. 

Case 12.— Tabic foot in a butler followed by progressive ataxy . 
Marked cutaneous sensory disturbances of the whole trunk , 
flaccid atony of abdominal muscles , with ballooning of the 
belly and drawing in of the lower ribs on inspiration through 
the unopposed action of the diaphragm. 

H. F., admitted to St. Pancras Infirmary 1898, aged 49, single, 
butler, denies syphilis, but has been in the way of getting it. 
When aged 38, first symptoms, ataxy and incontinence of urine. 
In 1897 spontaneous painless dislocation of right hip, Charcot’s 
joint, 1£ in. shortening of thigh. Occupation, heavy place, long 
hours, standing, and heavy manual work. 

Family history. —Nothing noteworthy, no history of previous 
illnesses. The following notes were made : 

Ataxic gait, ataxy in arms, muscles well developed, deep 
reflexes both of upper and lower limbs lost, superficial plantar, 
•epigastric, and cremasteric absent; marked hypotonus 10° beyond 
the vertical. Loss of joint sensation in legs and arms. Eyes : 
Two or three years before the ataxy, i.e., when he was 35, he saw 
Mr. Critchett for double vision which got better with a course of 
iodide. Pupils equal 2 mm. Argyll-Robertson, sight good. He 
suffers with frequent attacks of lightning pains in arms and 
legs, and girdle sensation. There is numbness of the hands and 
difficulty in buttoning his clothes. No tingling on pressure of 
the ulnar nerve. There is disease of the right tarsus, for the 
foot is much swollen in that part. It is of old standing, as 
it came on eighteen months before ataxy. 

The abdomen of this patient is enormously distended, the 
lateral portions hang down flaccid; the walls are like a thin mem- 



brane, devoid of fat and offering no muscular resistance. When 
the patient takes a deep breath, the lower ribs are distinctly 
drawn in, but the thin abdominal walls are bulged out by the 
intestines which are pressed forward by the descending dia¬ 

There was almost complete absence of light tactile sensi¬ 
bility over the legs and trunk up to the second space, extending 
a short distance down the upper arm on the inner side. There 
was a belt of analgesia over the fifth and sixth thoracic segments, 
and there was also analgesia of the legs extending half way up to 
the knees. In the same regions there was some thermo- 
anaesthesia. In other portions of the trunk and extremities 
where there was anaesthesia, there was either hyperaesthesia or 
hypaesthesia. Over the forearms and hands there were many 
hyperaBsthetic points, and in the right forearm, the seat of recent 
severe pains, were several greenish yellow pigmented areas with 
their long axes in the direction of the long axis of the limb, which 
he said were once bright red, and appeared when he had the 
pains. They no doubt correspond to the distribution of the 
terminal filaments of a sensory neuron, or group of neurons, 
which had been intensely irritated. 

The very marked sensory disturbances of the whole trunk 
indicated a very profound degeneration of the lower dorsal and 
upper lumbar roots, and this gave rise to a nearly complete loss 
of the reflex spinal tonus. The upper cervical roots are, however, 
not affected; consequently, the diaphragm is entirely unopposed, 
with the result the lower ribs are drawn in, and the flaccid 
abdominal walls protrude at each inspiration. He can contract 
the abdominal wall voluntarily, because the path from the cortex 
is still open to the spinal motor cells. If we assume that the 
posterior roots of the lower dorsal and upper lumbar segments 
contain sensory fibres from the intestines, there is probably a loss 
of reflex tonus of the intestines, and, in consequence, paralytic 
distension. He suffered some time ago with rectal crises, and for 
some time has required medicine to open his bowels. 

Case 13.— Argyll-Robertson pupils , history of hemiplegia , knee- 
jerk present on paralysed side , absent on the other.—(Hendon 
Infirmary .) 

J. T., aged 69 ; occupation basket maker; history of a right¬ 
sided hemiplegic attack ten years ago. Married at 30, no 
children, several miscarriages, history of syphilis, treated for some 



months with medicine. Pupils unequal, left a little larger than 
right, inactive to light, react to accommodation. Deep reflexes; 
knee-jerk obtained on the right side, not on the left; triceps ditto. 
Plantar reflexes and epigastric obtained on both sides, the former 
brisk. He has a hemiplegic, not ataxic gait. He has had no 
pains, and neither anaesthesia nor analgesia were discovered. 
He is, however, very feeble mentally. 

Case 14.— Advanced tabes , ataxy and cutaneous sensory disturbances , 
first symptom pronounced gastric crises , noio ceased . Brother 
died of general paralysis . 

C. P., aged 46, married woman, husband dead, now a nurse, 
no children, one miscarriage twelve months after marriage, 
second child only lived five months, no direct signs or history 
of syphilis. Symptoms began with gastric crises five years ago 
occuring every month or six weeks, followed later by a tight 
feeling round the waist. Two years later inability to stand or 
walk in the dark; three years ago she had a hystero-epileptic fit 
while in St. Mary’s Hospital; later she went into the Queen 
Square Hospital and received Frankel treatment without benefit. 
Four years ago she had bladder trouble. No neurosis or 
nervous disease in ftle family, except that her brother died of 
general paralysis, aged 33. 

Present state. —She can now get out of bed, but is unable to 
walk or stand without support, but she can wash and feed herself. 
The muscles are not wasted, there is marked hypotonus in both 
legs, deep reflexes of upper and lower limbs lost, superficial 
reflexes absent on right, just present on the left; epigastric, 
present on the right, absent on the left, frequently bilateral 
response to right-sided stimulation. Hyperaesthesia of skin over 
right side {vide fig. 8). There is a good deal of ataxy in the hands; 
she complains of great pains, shooting and darting in character, 
in the right infrascapular region. On moving, the pain was 
greatly aggravated, no friction was detected, although she thought 
she was suffering from pleurisy ; pain is in the region where 
hyperaesthesia is indicated in the chart. Joint sensibility lost in 
all joints of lower limbs and in fingers of upper. She has lost 
sensation in the ring and little fingers of the left hand within the 
last three months. She first became aware of this by a cramp¬ 
like feeling. She complains of a deep-seated burning pain in the 
epigastrium, but she does not now have gastric crises. Pupils, 
right 5 mm., left 3| mm., Argyll-Bobertson, complains of dimness 



of vision in right eye, but no facility for examination. The 
sensory disturbances are indicated in the subjoined chart. In the 
dotted area there was blunting of light tactile sensibility and some 
delay; in the black part there was no response to pricking or 
touch, in the cross-shading there was light tactile anaesthesia, and 
in the one-line shading, analgesia. 

Fig. 8. 

= Hypalgesia 
= Cutaneous Anaesthesia 

+ + + + 
+ + + + 

— Analgesia and Anaesthesia 
= Hyperaesthesia 

Diminished Cutaneous Sensibility 
to Pain and Touch 

Case 15.— Tabo-paralysis y dropping out of all the teeth , and 
absorption of the jaw . 

T. K., butcher, a patient in the Central London Infirmary, 
denied intemperance, also syphilis ; but there are well-marked 
signs on the body, scars on the prepuce, enlarged glands in the 



groin, large papery scara outside right shin. His work was that 
of a slaughterer and carrier. He has no friends, and his answers 
are unreliable as to family history. He can’t remember when he 
had to give up his work, but attended a hospital many years ago. 
He has a markedly ataxic gait, Romberg symptom, absent deep 
reflexes of both arms and legs. Plantar reflexes absent ; epi¬ 
gastric, right side brisk, left side present. Joint sensibility lost 
in toes and feet, hypotonus to a right angle. Pupils, right 1| mm., 
left 2 mm., Argyll-Robertson. He tells me all his teeth fell out 
not long ago, and there is great absorption of the alveolus in both 
upper and lower jaws. His mental state is such that his 
sensibility could not be tested with accuracy. He is unable to do 
the simplest calculation, his memory is very bad, mental reaction 
very slow, orientation in time and place very defective. He has 
a childish, fatuous expression, but his speech does not seem to be 
affected. There is no tremor of tongue or face. His mental 
condition suggests progressive dementia. 

Case 16.— Preataxic conditio7i, brisk knee-jerks , gastric crises , 
gradual development {with each successive crisis) of belt of 
thoracic ancesthesia. 

P. B., aged 37; packer in tobacco. No neuropathic family 
history. Definite history of syphilis sixteen years ago with 
secondary symptoms, for which he was treated eighteen months ; 
came to Charing Cross Hospital with paralysis of the right 
external rectus, Argyll-Robertson pupils, pains in the legs, first 
felt three years ago, history of several gastric crises, knee-jerks 
present and exaggerated, no Romberg symptom, no ataxy, no 
girdle sensation or difficulty with the bladder. Diagnosis, pre¬ 
ataxic tabes. Eighteen months later, July, 1901, was seen again, 
suffering with pains in the legs. There was no change in his 
condition noticed. There is no squint now, the knee-jerks are 
still brisk, there is no trace of ataxy and no hypotonus. A little 
later, I found a patch of anaesthesia corresponding to the posterior 
branches of the fourth and fifth dorsal roots on the right side. 
The anaesthesia came on after a series of gastric crises, with local 
pains. Three weeks later, he again suffered with a severe 
attack of gastric crises, and on testing the cutaneous sensi¬ 
bility, I now found a complete belt of cutaneous anaesthesia 
corresponding to the fourth and fifth segments as shown in the 
accompanying chart (fig. 9). 



= Cutaneous 


Case 17.— Tabo arthropathy. Gastric crises. Husband died in 
an asylum , of an acute brain disease , at the age of 36, very 
probably general paralysis. 

B. C., aged 53, an inmate of Lewisham Infirmary, married at 
17, no children born alive by the first husband ; four months after 
marriage, miscarriage; (2) miscarriage six to seven months; 
(3) miscarriage four months; she has always been in good health, 
she gives no sign or history of syphilis, except the history of 
miscarriages, and the existence of a pigmented scar t size of a 
half-crown, over the upper part of left buttock. Her husband 
died five years after marriage, at the age of 36, in an asylum, of 
acute brain paralysis. She remained a widow four years; 
married again, and had no children by her second husband. 

Occupation. —After second husband died, she worked a heavy 
sewing machine for four years. She struck her knee against the 
wheel, and pain in the knee followed, but she had to go on work- 



mg the machine to earn her living. The knee swelled up, but 
caused her no pain, she went to the hospital, and the surgeon 
informed her that it would have to be amputated, which surprised 
her very much. A year later, it was taken off at St. Thomas’s 
owing to the foot beginning to swell. Mr. Shattuck has informed 
me that it was a Charcot joint. There were no signs of ataxy then. 
After leaving the hospital, she worked a hand machine for three 

Diminished Cutaneous Sensibility 
to Pain and Touch 
Prick Felt as Touch 

or four months, but she was obliged to give it up owing to attacks 
of sickness. These attacks came on independently of food. At 
the time she had her leg off, she had the Argyll-Robertson pupils, 
but no affection of the bladder or bowels. 

Physical condition .—Pupils unequal A.R. right 3 mm.; left 
5 mm. Colour vision good. No contraction of fields. Reads small 
print. No affection of other special senses. Musculo cutaneous . 



—Feeling of wool on the sole of the foot. Pins and needles of 
left hand. Marked loss of sense of position in joints of lower 
limb; not marked in hands. No great amount of muscular 
wasting, but marked hypotonus of left leg. Knee-jerks absent. 
For sensory disturbances of skin, vide charts. Visceral symptoms 
—She is subject to very severe gastric crises, which are preceded 
by intense occipital headache, and a feeling of distension of the 
stomach, and this is followed by attacks of lightning pain through 
the whole body ; this pain does not however extend beyond the left 
knee , but into the stump of the right knee. It affects the left 
arm and fingers more than the right. The pain lasts from one to 
three days, and she is in the greatest agony. She gets no relief 
until she has taken a large dose or two of trional. . She can’t 
bear the light to the eyes, and has to lie on her face during the 
attack. She obtains no relief by hot bottles or fomentations. 
Swallowing ice gives some relief. She has on occasions vomited 
coffee ground matter, but never bright blood, and she has experi¬ 
enced relief afterwards. This was her own voluntary statement 
without the need of any questions being put. She has only one 
tooth in the upper jaw, and two in the lower. She tells me that 
they have all dropped out. Two years ago five dropped out in a very 
short time. Dr. Toogood (to whom I am indebted for this case) 
tells me that at various periods this patient has had patches of 
erythema in various parts of the body, following or associated with 
the crises. The complete loss of sensibility to all forms of painful 
stimulation in the left leg, coupled with the fact that this is the 
only part of the body in which she does not suffer pains during 
the crises, suggests the probability that the third, fourth, and 
fifth lumbar, and the first and second sacral roots are destroyed, 
and probably also the association neurons of the substantia 
gelatinosa in these segments. 

Case 18.— Female . Definite syphilitic history , tabo-arthropathy , 
other symptoms of tabes slight. Cutaneous ancesthesia of 
fourth segment , but posterior divisions unaffected. 

A. C., aged 57, married at 24, no children living, four 
pregnancies : (1) miscarriage six months after marriage; (2) bom 
dead twelve months after marriage; (3) born dead; (4) mis¬ 
carriage. Says that she had good health all the time, but hair 
came out soon after marriage ; she suffered with sore throat and 
(rheumatic ?) fever. 



History of illness .—First symptom was a swelling of the left 
knee twelve years ago, came on gradually, very painful, she 
attributed it to kneeling as a charwoman. She*went on using it 
to kneel on for eight years. For the last ten years she has 
suffered with pains in the legs. She had no ataxy. Two and a 
half years ago her left leg was amputated for Charcot’s joint. A 
little later the right knee began to swell; it was very painful, and 
she had to come into the infirmary again. She complains now of 
pains in the hand, and she has marked ulnar deviation and 
typical rheumatoid arthritic affection of the phalangeal and meta- 

= Cutaneous Anaesthesia 

carpophalangeal joints. The deep reflexes, triceps and knee-jerks 
are absent. All the superficial reflexes are present. There are 
many papery scars over the back and legs ; the right knee-joint 
is much enlarged, there is considerable fluid in the joint, and it is 
painful. She suffers with no ataxy of hands or feet, or loss of 
joint sensation. Cutaneous sensibility (see chart). Note pos- 



terior division of fourth thoracic root not affected. Vision good, 
colour vision good. Three years ago she suffered with transitory 
diplopia. Pupils equal, 4 mm., A.R. 

Case 19.— Ataxy , impotence with anaesthesia of genital organs and 
anal region , pointing to destruction of sacral and coccygeal 
roots . 

R. D., aged 38, carpet planner, admitted for unsteadiness in 
walking, shooting pains in legs, and tightness round the waist. 

Family history.—nil noteworthy, no neuropathic heredity. 

Personal history. —Married fifteen years. His wife has had 
nine children, six of whom are living. 

Previous illnesses. —Syphilis two years before marriage, seven¬ 
teen years ago suffered with hard chancre for which he was 
treated for two months. Patient has led a hard life, he has 


been a carpet planner since he was twenty years of age. 
Moderate alcohol. 

Present illness .—Began about a fortnight after recovery from 
influenza, January, 1900, by shooting pains in both legs and pain 
in the head of a morning. Between the attacks of pain he 
noticed numbness of the legs, and felt as if he were walking upon 
felt. He commenced to be unsteady in his gait, and frequently 

= Cutaneous Anaesthesia 

= Hyperaesthesia 

Analgesia and Anaesthesia 

Diminished Cutaneous Sensibility 
to Pain and Touch 

pitched forward as if his knees had given way. About this time 
he had very little power in retaining his urine, which would 
dribble away unless he frequently relieved his bladder. One 
month after the onset of the first symptoms, patient felt a 
numbness in the anal region, and he became very constipated; 
had also pain in the perinaeum, especially when he micturated. 



Feeling of constriction round the lower part of the abdomen for 
the last six years, not worse lately. Complete failure of sexual 
power for the last six months. No gastric, laryngeal, or nephritic 
crises. Muscular power unimpaired, some hypotonus of ham¬ 
string muscles. Sensation :—Considerable impairment of tactile 
and painful sensations in regions indicated in chart, but thermal 
sensibility unimpaired (figs. 12 and 13). Muscular sense 
unimpaired. Very slight incoordination of upper and lower 
extremities. Gait:—Patient walks steadily without a wide base 
of support, turns round fairly well, but slightly unsteady. 
Romberg’s symptom fairly marked. Pupils equal, somewhat 
dilated, Argyll-Robertson. No paralysis of the external ocular 
muscles. Reflexes:—Knee-jerks and triceps jerks absent on both 
sides. Epigastric, cremasteric, and plantar reflexes sluggish. 

Case 20.— Blind. Third stage of tabes , all the roots practically 
almost destroyed except the upper four cervical. The charts are 
interesting as showing the wider distribution of analgesia , and 
the more limited distribution of thermo-ancesthesia. The sharp 
line of demarcation of tactile anaesthesia is of interest . He is 
unable to converge the eyeballs , although he made the effort to 
do'so and thought he had succeeded.—(Cleveland Street 

H. D., aged 50, mill band maker, hard manual work, single, 
does not know cause of his illness. Thirty years ago had a sore 
on the penis, which he treated himself with lotion; glands in the 
groin, hard shotty, no signs or scars on the body. In 1882, he 
suffered with cold feet and pains in the legs, followed by difficulty 
in walking, double vision, and inability to distinguish colours. 
He had to give up work in 1883, because he was too unsteady on 
his legs, sight progressively became worse, and six or seven years 
ago he became quite blind. About this time he also had difficulty 
with his water. He is now quite unable to stand, walk, or feed 
himself, partly because of the loss of sense of position and partly 
through muscular wasting and weakness. He is much emaciated , 
the feet are very cold and in a position of talipes equino varus; 
they are cyanosed, and the skin smooth and glossy. He is unable 
to turn himself over in bed, and is quite helpless. All the deep 
and superficial reflexes are lost in the limbs, and there is marked 
hypotonus. He has no joint sensations, and he cannot tell 


whether there is anything in his hands or not when it is put 
there, and the only way he knows is to put the object up to his 
lips and feel with this sensitive part of his body. Thus I put the 
percussion hammer in his hand, made him clench his fingers 
(he held it between the ring and middle fingers with the fist 
closed), but not till he had put his lips to it could he tell me that 
it had a stem. He is absolutely blind, right pupil 6 mm., left 

Fig. 14. 

= Cutaneous Anaesthesia 

5 mm., cataract right eye, both pupils inactive to light and pain, 
and hardly any movement on convergence. On being told to lift 
up his left hand and look towards it, the right eye remains 
immobile. The left moved towards it, and then immediately 
swung back by oscillations to the straightforward position. The 
patient thought that he was directing his eyes to the hand all the 



time he was making the effort to do so. He was unable to con¬ 
verge the eyes to the position required for looking at the nose, 
although he made the effort, and he was rather surprised when 
I told him that he had not moved his eyes. He has no affection 
of taste or smell; the cutaneous sensibility is indicated in the 
accompanying charts. It may be mentioned that there is always 

Fig. 15. 

= Hypalgesia 

= Analgesia 

considerable delay where sensation is felt at all, generally in¬ 
correct localisation, sometimes allochiria. There is a good deal 
of variation with regard to response to stimuli, as if the stimulus 
was sometimes insufficient to rise into consciousness, the stimulus 
sometimes became apparent by repetition and summation. Places 
where formerly he felt prick of pin were afterwards not felt, while 
other places were. 



o o o o 
o ° o o o 

non w 


+ ++ + 
+ + + + 

= Hypersesthesia 
to cold 

Case 21.— A case of tabes to show extension of ancesthesia over one 
side of thorax and down inner side of left arm , showing unequal 
affection of the roots on the two sides.—(Bethnal Green 

E. M., aged 34, widow, charwoman. Married at 19, no 
children, never had any, history of three miscarriages, first being 
four or five months after marriage, marks of old syphilitic erup¬ 
tion on the body, and a squamous syphilide. Symptoms com¬ 
menced two years ago with a giving way of legs, lightning pains 
and bladder trouble. She can walk fairly well, knee-jerks are 
absent even on reinforcement, there is considerable hypotonus in 
the thigh muscles, deep reflexes lost, superficial present. Pupils, 
irregular, slightly unequal, about 5 mm., very sluggish reaction to 
light, react well to pain and accommodation. 

Cutaneous sensation. —There is anaesthesia and hypaesthesia 
over the left side of the thorax and extending down the inner 
side of the arm. There is a belt of cutaneous anaesthesia, as 



shown in the diagram, and in this region there is hypalgesia. In 
the feet there is hypcesthesia and hypalgesia. Loss of joint 
sensation in toes. 

Analgesia and Anaesthesia 

|= Cutaneous Anaesthesia 

Diminished Cutaneous Sensibility 
to Pain and Touch 

Case 22.— Female . History of syphilis from husband at 18 ; 
married second husband four years later , miscarriage , ulcer¬ 
ated legs , rectal crises , bladder troubles , and symptoms of 
mild gastric crises , loss of use of legs , symptoms of pro¬ 
gressive tabes , marked cutaneous disturbances of trunk and 
lower limbs progressing rapidly with severe pains y loss of 
bone sensibility in same region as cutaneous disturbances . 
Mental depression , attempted suicide . 

C. A., aged 37, married woman, went to the Obstetric Depart¬ 
ment of Charing Cross Hospital, and was sent on to me. 

Personal history .—Married at 17 to a retired naval man; 
eight months’ child born, lived only two days. She found that 
her husband suffered with venereal disease, she had a sore 



throat and her hair came out; she therefore left him. After his 
death, she married again at 22 a retired soldier. Miscarriage four 
months after marriage, leaving her with uterine disease. Subse¬ 
quently she suffered from ulcerated legs, and had two more 
miscarriages. She noticed first a feeling of a cord round the 
waist, then rectal crises, and difficulty in holding her water two 
years ago, for twelve months pains in the legs and body, and 
progressive difficulty in walking. Frequent attacks of giddiness 
and flatulent eructations with gastric distension. 

Black indicates the bones which are insensitive to the vibration of the 
tuning fork. The third and fourth ribs were not absolutely insensitive. In 
-distribution the loss of bone sensibility in this case corresponded pretty 
closely with the cutaneous anaesthesia. 

Physical signs .—Pupils equal, small, A.R.; absence of deep 
reflexes, plantar reflexes lost, epigastric just present, cutaneous 
anaesthesia from fourth to tenth segments inclusive, anaesthesia 
and paresthesia of soles of the feet, analgesia or hypalgesia to 
pricking of legs, and of the thorax from fifth to ninth segments, 
with some hyperaesthesia above and below. Marked incoordina¬ 
tion and wasting of legs, no incoordination in hands. Marked 
hypotonus of hamstring muscles. 



Two years later she became quite helpless, the cutaneous 
disturbances had become more marked. Slight contraction of 
field of vision, and pallor of discs. Retching attacks without 
vomiting, epigastric pain. Foot drop from paralysis of dorsal 
flexors, some inversion of soles, especially of right foot, from per¬ 
oneal paresis. Loss of bone sensibility, as shown in the above 
chart. She is now very depressed because she fears she may 
give her husband the disease. She has attempted suicide. 

Case 23.— Ataxy without anaesthesia , loss of sense of position, with¬ 
out loss of joint or bone sensibility . 

H. M., aged 39. Occupation, warehouseman. Married, no 
children, one miscarriage three years ago. Contracted syphilis 
in 1886, treated for several months, well-marked secondary 
symptoms. No neuropathic or psychopathic history in family. 
For four or five years, suffered with pains in the legs. During 
past year has had difficulty in starting micturition, bladder not 
emptied. Difficulty of walking in the dark and .sways with his 
eyes shut. For some time past has noticed that his legs would 
suddenly give way, feeling of constriction round the waist, shooting 
pains up the spine and down the legs, but never extending to the 
head. Gastric crises, attacks of palpitation, rectal crises, and 
laryngeal crises. While in the room he had an attack of laryngeal 
spasm and dyspnoea. Sight not so good as it was. 

Physical examination —Deep reflexes lost. Ataxic gait first 
stage. Pupils unequal, A.R.; abdominal and plantar reflexes 
exaggerated. No cutaneous anaesthesia discovered, hyperalgesia 
over the thorax and in the legs. Bone sensibility unimpaired, 
joint sensibility unimpaired. Some general loss of weight. 
Hypotonus moderate of hamstrings, no muscular wasting. No 
foot-drop when lying on back. Considerable static ataxy in legs. 
Commencing grey atrophy of both discs. 

GROUP 2.—Gases of Tabes with Insanity. 

Case 24.— Tabes (? tabo-paralysis), with grandiose delusions , 
mania a potu , auditory hallucinations , analgesia . Tabic foot . 

J. B., aged 38, admitted to Hanwell, April 2, 1900, occupation 
musician, single, duration of attack two weeks. He was admitted 
to the asylum in a very excited, restless, talkative, and threatening 
condition. He states that he is the greatest composer and flute 
player in the world. He fancies he has £80 in his pocket, which 
is not true, also that he possesses great wealth, horses, carriages, 



&c. He talks incoherently of solicitors, detectives and numbers 
of police at his command. He has been employed in the orchestra 
of a theatre and he has led a very irregular dissolute life. Diagnosis 
was mania d potu and probably tabo-paralysis. 

Personal history .—He has twice before suffered from melan¬ 
cholia, the first attack occurring seventeen years ago. 

Family history .—Mother died of phthisis, and father of para¬ 
lysis, aged 61. Family history of intemperance. Patient’s relatives 
very neurotic individuals (Dr. Alexander). 

Medical examination .—Tongue coated, very unsteady, pupils 
equal and react to accommodation, not to light, knee-jerks absent, 
history of syphilis with small scar on penis. 

In August, 1900 when I saw him he was in the following con¬ 
dition :—Stepping gait, but can manage to get upstairs, absent 
knee-jerks, hypotonus in legs, Romberg’s symptom. He has an 
enlargement of the tarsus on the right side. He is much quieter, 
mentally, than he was, sleeps well and is quiet and well-behaved. 
There is no tremor of tongue or lips, and no affection of speech is 
noticeable. Patient can give a good account of himself and his 
family, and his knowledge of time and place are alike good. The 
only evidence of insanity is a certain amount of loss of control and 
the repeated statement that he hears electric wires playing con¬ 
tinuously. When questioned about this, he whistled an air from 
an opera to indicate the tune which the wires were playing. He 
was much astonished that I did not hear this music, but his listen¬ 
ing attitude and expression convinced me that these auditory hal¬ 
lucinations were very real to the patient, and that what he was 
whistling was actually what he heard. In testing his sensation 
it was found that he did not feel the point of a needle except as a 
touch in any part of his body. After some delay he recognised 
a hot spoon. He has no girdle sensation and no visceral crises. 

October 24. Further improvement, sent out on trial. He 
was not heard of again. 

Case 25 .—Tabes dorsalis , with ataxy and left crural mono¬ 
paresis, auditory hallucinations , systematised delusions of 
persecution associated with the pains ; little or no dementia . 

F. W. R., male, aged 35, single, clerk; admitted to Claybury, 
September, 1899. 

Family history .—Mother died in asylum, father attempted 
suicide, died of gangrene. 

Personal history .—Gonorrhoea several times, syphilis at the age 
of 26, urethral chancre, followed by syphilitic eruption treated for 



five months. Two years ago right great toe removed for diseased 
bone. He began to feel electricity in his legs about two years ago. 

Mental state .—“ Female enemies follow him about; they work 
the electricity on him; the whole thing is going on owing to a 
jealous woman, who has followed him from Plymouth to 
Homerton, thence to Claybury.” He hears female voices talking 
every night; they talk to one another, and he gets quite con¬ 
fused and helpless ; they are the voices of two nurses from 
Plymouth; he is watchful, and “ has to keep his eyes open ” ; 
his memory and orientation are good, and he can talk on most 
matters quite sensibly. 

Physical state. —On both shins numerous old circular punched 
out scars of former syphilitic ulcers ; cervical glands shotty; 
pupils equal, 2| mm., react slightly to accommodation, doubtfully 
to light. Knee-jerks absent; sensation is dulled and delayed in 
the feet and legs, but localisation fairly normal. Bight mid-thigh 
measured 12 ins. in circumference, left, Ilf ins. Bight mid-calf 
is 8i ins. in circumference, the left, 7f ins. There is no loss of 
sense of position or cutaneous sensibility in the arms, but reaction 
time is lengthened. Plantar and abdominal reflexes present. 
He can hardly stand with his eyes open, and would fall when 
they are shut; his gait is tabetic; he stamps with the right foot 
when walking, and drags the left foot after him; there *s 
hypotonus in both legs ; there is some fine tremor of the tongue, 
but no jerking; there is no tremor of the face or lips, and no 
affection of speech. Later he developed a slight external squint 
in the right eye. 

I saw this patient August 30, 1901. He walks with a wide 
base; heels down first, throws the right leg forward like a 
hemiplegic man, dragging the paretic left. He is unable to stand 
or walk without assistance; all superficial reflexes present; 
triceps and knee-jerk absent; sense of position lost in toes and 
ankle of right foot, not in left. Pupils, 3 mm., trace of light 
reaction in the right eye, none in the left; accommodation in both 
eyes. Cutaneous hypaesthesia in the area of the fifth thoracic 
segment; hypaesthesia and hypalgesia of the right foot, none in 
the left. 

Mental state. —He answers questions quite rationally, but tells 
me that he hears voices at night talking to him; they are those 
of women, one particularly, a nurse, who continually annoys him, 
not only by what she says about him, but by causing him to have 
electric shocks in his limbs, body, and face. They pull his bowels 
about, and cause him to have pains at his heart; some time ago 
they continually put poison into his rice pudding, which burnt the 



inside of his stomach. He has nothing to complain about his 
food now; his senses of smell and taste are both good (tested), 
also his hearing in both ears (tested). 

April, 1902.—Physical condition shows little change, except 
that the general health is better. He is still very ataxic, and 
walks with a hemiplegic gait; his sensibility to light tactile 
sensations on the chest showed at first anaesthesia, but after 
repeated observations it became only a condition of hypaesthesia 
of the sixth, fifth, fourth, third, and second dorsal root areas, the 
anaesthesia extending down inner side of the upper limbs as far as 
the middle of the forearm. The better appreciation of the 
cutaneous stimulus was no doubt an effect of summation. While 
performing this test his eyes were covered, and he was requested 
to put his finger on the spot touched. A metronome was beating 
at the time, and he said that he heard voices say to him, “ You 
have been a lunatic to have gone away from Sydney Street.” 
Last year he made the same statement when the metronome was 
set going, and he said it in rhythm. He hears the female voices 
especially at night, but also in the airing court, where they 
appear distant, but very real; when I spoke of them as hallu¬ 
cinations he was much disturbed. He has the same delusions 
that the people whose voices he hears torture him with electricity, 
and unasked he said “ that they had now turned the electricity 
on to his arms,” affecting his ring and little finger, which is of 
interest, seeing that the cutaneous anaesthesia has now spread to 
the arms, indicating thereby degeneration of the lowest cervical 
and uppermost dorsal roots. He says that “ they pull his legs at 
night,” which is, no doubt, an insane interpretation of spasmodic 
cramps; there is loss of joint sensation in the ankle and toes, 
specially in the right, by a failure of the synergic action of the 
dorsal flexors of the foot when the hip is flexed; considerable 
hypotonus in the legs ; no affection of speech. 

Case 26.— Early tabo-paralysis, (probably) drink. Delusion of 
wealth. Hallucinations and delusions respecting his zuife ivho 
committed suicide. 

S. J. P., aged 36, admitted to Hanwell, August 8, 1901. 
Occupation, coachman ; married, no children. 

Family history .—Father and mother died when young, no 
history of insanity or consumption obtainable. Brother and sister 
alive and well. 

Personal history. —Since wife committed suicide eighteen 



months ago, he has drunk a good deal. Up to then he had been 
quite healthy and temperate. About three months ago he 
suddenly developed ideas of wealth, and made all manner of 
statements with regard to the great deeds he had performed. He 
has always been good-tempered but excitable. History of 
chancre, treated at Lock Hospital four years before marriage. He 
has many delusions of wealth and grandeur; also that his wife 
has come to life again, persists that he saw her last Saturday 
week, and that she has been seduced by numbers of people. He 
knows where he is, the time of the year, and beyond the delusions 
mentioned, gives an accurate account of his previous life. 
Speech is unaffected, and there is no tremor in the lips or tongue. 
There is no ataxy, the right knee-jerk is absent, the left just 
obtainable. Pupils irregular, 3£ mm., Argyll-Robertson. No 
cutaneous anaesthesia. 

He made the following statement to me :— 

His wife came both to St. Pancras Infirmary and to Hanwell 
to see him, she was fairly well dressed, and looking well. She 
is now an actress at New York, but had never been an actress in 
England. She was buried from her own house, and he worried 
about her, and said he would have the coffin opened, and when 
they got there, they found the coffin empty. When she came 
to see him she had nothing on except a shirt, and a Mr. P. gave 
her clothes and took her straight out to New York. He has 
written a letter, but it has been returned. I asked him, “ Did 
she talk to you when she visited you.” He replied: “ Yes. She 
said: ‘ We shall not have the old happy days over again,* ** he 
said, “ It was certainly not a dream.** 

April 1902.—Physical condition good, but he still persists that 
his wife is alive, and visits him occasionally, and that he knows 
she is not dead, for he had the coffin opened, and it was empty. 
He will talk quite rationally on other matters. 

October 28.—Slight tremor of face and tongue, expression of 
early general paralysis. Slight dementia. He has now lost 
delusion about his wife. 

Case 27.— Tabes , optic atrophy , ataxy first stage , formication and 
sensation of ivater trickling in his skin , which he believes is 
the medicine he had at the London Hospital . Trunk 
anaesthesia and hypalgesia. Later crises either lamygeal or 
cardiac . 

J. D., married, aged 24. Denies ever having syphilis, but 
has been in the way of getting it, admits that he had a veneral 
sore, not treated. His wife has had four children born alive, of 



which two are dead ; one born dead, and three miscarriages. 
There is an inherited neuropathic history on the father’s side. 
Patient himself has always been an anxious man ; good husband, 
and good father, not addicted to alcoholic excess. He has com¬ 
plained for the last five years of rheumatic pains in his legs, and 
two months ago was unable to use his right arm on waking in the 
morning. He noticed that vision in his right eye was greatly 
impaired. For some time past his wife states, that he used to 
come home after his work greatly fatigued, and wanted to sleep. 
She never noticed any strangeness in his manner. He was 
always quite sane and rational, although very depressed. His 
wife noticed that he has had a staggering gait for more than six 
months past. Three weeks ago, he went to the London Hospital 
on account of his affection of sight. The curious sensory phe¬ 
nomena that he now complains of, he had then, and at first it 
was thought, specially as he had concentric limitation of the field 
of vision on the right side, that his disease was of hysterical 
nature. The Argyll-Robertson pupils, the gray atrophy, the 
absent knee-jerks and his mental depression led Dr. Head to 
consider the case to be either one of tabes with mental crises, or 
early tabetic general paralysis. He was sent to the Whitechapel 
Infirmary, and transferred to Claybury. He describes what took 
place when he appeared before the magistrates and was certified, 
and persists in the statement that he feels the sensations he 
described, that they are no delusions, and that owing to his 
having stated these sensations as being real, and due to the 
medicine he had given to him in the London Hospital, the 
magistrate was satisfied as to his insanity. He relates that 
another patient in the infirmary ward, told him that even if he 
felt those sensations he should not have mentioned them, but u he 
had to speak the truth.” This morning, September 25, he said 
that he had the feeling of water trickling down his right leg, and 
a sensation as if his foot were swollen. He may have had this 
sensation ; when, however, shown the right foot, and asked to 
compare the size and appearance with the left, in which he 
had the sensations described, he expressed himself as perfectly 
aware that his sight told him that there was no difference. He 
converses quite rationally on all subjects and displays no incoher¬ 
ence. His speech is not hesitant, nor is there any tremor in the 
tongue or lips. There is however, an expression denoting loss 
of tone in the muscles of the face, as if there were depression of 
the emotional centres. It may be, however, that this facial 
expression is partly due, as he says, to anxiety in being placed in 



the asylum ; his wife and children having no means of subsis¬ 

He also complains of this curious trickling (formication) 
coming up bis back and over his head and to his forehead, but 
not on to his face; it travels also down his arms to the hands; 
he thought it was the medicine that he had in the London 

October 27, 1901.—Severe girdle sensations, which he de¬ 
scribes as if something was squeezing him in a vice. 

Patient looks well, good nutrition. He complains that he has 
had shooting pains in the upper part of the chest two or three 
months ago, but these have now passed off, and he now feels at 
night a sense of tightness and difficulty of breathing, with a 
feeling of soreness. It wakes him up with a struggle to breathe. 
It catches him in the throat. All over the whole head he has a 
feeling of tightness. When it comes upon him he feels as though 
thousands of needles were working upon him. He is obliged to 
take medicine to keep his bowels open. He complains also of 
burning feelings both in passing his water and motions. Passes 
his water pretty freely. No hallucination or delusions ; recognised 
me perfectly. Has nothing to complain about food or treatment. 

Speech is not affected. Sways a bit with his eyes shut. Can 
touch the tip of his nose with forefinger of both hands, has no 
ataxic gait. He says himself that he has a tendency to fall either 
one way or the other. Pupils equal, 4 mm., inactive to light, 
react to accommodation. Some limitation of the field of vision of 
the right eye in the upper and inner parts. Colour vision of the 
right eye somewhat considerably impaired, recognised yellow, 
not red, green or blue. Slight tremor of the tongue, slight tremor 
of the lips. He has rather a dull, heavy expression. There is a 
belt of cutaneous anaesthesia corresponding to the third, fourth, 
fifth, and sixth segments, with some hypalgesia in this region. 
On the feet and lower part of the legs and over the lower part 
of thorax and epigastric region there is some delay and 

March 18, 1902.—The chart of the cutaneous anaesthesia has 
not appreciably altered. He still suffers with attacks of severe 
pain, which he says is like electricity ; he also suffers with attacks 
resembling in some respects angina, which Dr. Jones says are of 
the nature of cardiac crises. The patient described the attacks 
to me as follows :—“ He has always a feeling of a band around 
the chest, but at times it is as if it were being tightened up, 
making him unable to breathe, and necessitating him assuming a 


sitting-up posture.” The feeling of constriction, he says, spreads 
to his throat as if he were being choked (laryngeal crises?). This 
sensation is accompanied by severe pains shooting all over his 
body. He still has the feeling he described on admission as of a 
trickling of a fluid under his skin spreading up the back of his 
head over his forehead and on to his face. He believes that this 
feeling is associated with a swelling of the cheeks. Mentally he 
has not changed, there is no sign of dementia. 

Case 28.— Tabes of sixteen years' duration , commencing with optic 
atrophy, followed soon after by mania with delusions of perse¬ 
cution ; subsidence of acute mental symptoms and gradual 
development of spinal symptoms , which after ten years led to 
helpless ataxy, mental enfeeblement, but no progressive de¬ 
mentia. Death from acute dysentery. Tabic lesion of spinal 
cord and roots, in cervical and lumbo-sacral regions, especially; 
affection of both exogenous and endogenous posterior spinal 
systems ; marked patchy pia-arachnoid thickening over pre¬ 
frontal, frontal , and central convolutions ; chronic atrophy of 
superficial layers of fibres and cells of cortex in these regions 
without vascular changes . Was this a case of mania and 
tabes, or tabetic general paralysis with arrest of mental 
symptoms ? 

C. R., aged 38, admitted to Colney Hatch in 1886 for mania 
and delusions of persecution. He had lost right eye when a 
youth as a result of injury. Some months before admission to 
asylum the sight in the left eye began to become dim, and he 
rapidly became completely blind. By occupation a colourman, 
the question of lead-poisoning was considered as a cause of his 
affection. There was no history of syphilis obtained, nor were 
there any signs on the body. The cause of the attack of mania 
was associated by his friends with the worry caused by the loss of 
sight. While in the asylum and after the subsidence of the attack 
of mania, ataxic symptoms developed, and in 1897 I first saw him 
in good physical condition, although he was in the third helpless 
stage of ataxy. He was unable to stand without assistance, and 
had to be supported by two attendants when he walked. All the 
deep reflexes were lost. The plantar reflexes were lost, the 
gluteal present on the right, absent on left, epigastric reflexes 
increased ; cremasteric absent. The muscles are well developed, 
and the muscular strength is good ; there is considerable hypo- 
tonus in hamstring muscles, the limb can he raised when extended 
at the knee to a right angle with the body. 



Sensation .—He does not complain of pains, numbness, or 
formication. There is diminution of sensation and delay to all 
forms of stimulation, with very incorrect localisation in the feet 
and legs. Over the abdomen and thorax there is apparently 
some hyperaBsthesia, especially to cold, but no anaesthesia or 
analgesia. He has no loss of sensation, painful or light tactile in 
the tips of the fingers, but there is a loss of sense of position in 
the joints. There is marked loss of sense of position of the joints 
of the lower extremities. The left pupil is dilated, and reacts 
neither to accommodation nor light. There is well-marked 
primary atrophy, with cupping of the disc. 

Visceral .—He is unable to retain his water which dribbles 
away from him ; there is no history of gastric or other visceral 

Mental .—He is somewhat weak-minded, but will converse 
about general topics, remembering the visits of his friends and 
what they said, and the day of the month. His comprehension 
is fair and he answers questions rationally; occasionally he is 
subject to violent outbursts of temper, but he has no delusions 
or hallucinations. There is continually twitching of the facial 
muscles and of the left orbicularis palpebrarum. He has no 
hesitancy or slurring of speech and the dementia has not been 

The patient remained in statu quo until an outbreak of 
dysentery occurred in his ward; he was sick, took to his bed 
and passed a large quantity of blood and slime, be<?ame very 
anaemic and collapsed and died in two days. At the post mortem , 
I found the whole of the large bowel and the lower twelve inches 
of the small bowel filled with blood and slime ; there was no 
ulceration anywhere in the alimentary canal to account for this ; 
the mucosa and sub-mucosa were greatly swollen and congested 
and, microscopically examined, showed the characteristics of the 
very acute fatal form • of dysentery. The other thoracic and 
abdominal organs were healthy with the exception of some 
atheroma of the aorta. The brain weighed 46 ozs., there was not 
much sub-arachnoid fluid, but there was considerable pia-arachnoid 
thickening over the frontal and central convolutions on both sides. 
There was especially thickening of the membranes and atrophy of 
the superior parietal lobe, just behind the upper fourth of the 
ascending parietal, and on stripping the membranes, a shallow 
pit, 1 in. square was seen, due to this atrophy, symmetrical 
in both hemispheres. The lateral ventricles are faintly granular 
and not dilated ; the fourth ventricle is somewhat dilated and 


(P) U) 

Section of superficial layers of ascending frontal, showing (A) Molecular 
layer and small pyramids; (B) medium sized pyramids. Magnification 
180 diameters. 

Tabes in Asylum and Hospital Practice. 

To face p. 125. 


[(C) ( B) (A) 

(A) Thick section of cortex (ascending parietal) with adherent pia-arachnoid which is greatly- 
thickened, and consisting in this situation of a series of strata of dense fibro-vascular tissue. The 
tangential and supraradial fibres in the subjacent cortex are diminished considerably, but the 
section is too dense to show this properly. 

(B) Thinner section of cortex (ascending frontal). Membranes not so much thickened, a fair 
number of tangential fibres seen. 

(C) Deeper layers of cortex (ascending parietal) showing radial, supraradial, and interradial 

Magnification 150 diameters. 

Tabes in Asylum and Hospital Practice. 

To face p. IS 5. 



there are some granulations. There is slight thickening of the pia- 
arachnoid over the superior temporal convolutions and along the 
tip of the temporal lobe, and the anterior part of the uncinate 
convolutions. The thickening of the membranes and atrophy of 
the convolutions is more apparent in the upper two-thirds than 
the lower third of the central convolutions. 

Preliminary microscopic examination of the brain by Nissl and 
Weigert methods of staining cells and fibres showed the following 
conditions :—The small cells of the molecular layer of Cajal are 
greatly diminished in places; also, but to a less degree the small 
pyramids, and less still the medium sized pyramids. Those cells 
that remain of the pyramidal layers have a fairly normal appear¬ 
ance and are arranged in columns with straight apical processes 
which can be followed for some distance. The large Betz cells 
lying in small groups of four to six are for the most part quite 
normal, they have all their processes, and the majority of cells 
present no chromophilous changes. Portions of the first frontal, 
ascending frontal, and ascending parietal, stained by Wolter’s 
method for fibres show thickening of the pia-arachnoid of con¬ 
siderable degree and proportional to an atrophy of the tangential 
and supra radial and interradial fibres, quite as marked as in a 
case of fairly advanced general paralysis. There are no vascular 
changes, no plasma cells, and comparatively little glia cell prolifera¬ 
tion (vide photo-micrographs, Plates I. and II.) The complete 
examination of this brain will occupy the subject of a future 
communication, being one of considerable interest. Is this a 
wasting of physiologically correlated structures in a case of 
tabes, or is it the lesion of a case of arrested general paralysis ? 
When such difficulties of diagnosis exist, as in this case, one is 
impressed by the unity of the two diseases. 

Microscopical examination of the spinal cord .—The degeneration 
in the spinal cord corresponded fairly accurately with the clinical 
symptoms observed during life. The cord was, with the exception 
of the posterior columns, of normal size, the myelin sheaths, unlike 
many tabo-paralytic cases, stained remarkably well. There was 
no degeneration of the pyramidal systems of fibres to be found 
anywhere. The atrophy was limited to the posterior roots and 
posterior columns of the cord. There is almost complete dis¬ 
appearance of the fibres of lumbo-sacral roots forming the cauda 
equina. The upper four lumbar and the last four dorsal roots at 
attachment to the cord possess still a large number of healthy 
fibres ; in the mid and upper dorsal roots the fibres become less 
and less numerous until the cervical region is reached. At the 



seventh cervical there is a great increase in the number ot 
fibres, and above this level the number is normal, and there is 
abundance of fibres in the cornu radicular zone. 

Spinal cord .—The column of Goll is completely denuded of 
fibres in the cervical region, except a A shaped portion in front, 
which corresponds to the lower dorsal and upper lumbar roots; 
in front of this area of fibres there is a A shaped area of sclerosis 
which corresponds to the outfall of fibres in the upper dorsal and 
lowest cervical roots. Examination of each segment of the cord 
shows that this most ventrally placed A shaped area of sclerosis 
corresponds to the outfall of fibres coining from the upper three 
dorsal and last cervical roots. These represent fibres which 
carry impulses from the deep structures, muscles, and joints 
of the hand. Thus at the eighth cervical We find a complete 
atrophy of entering root-fibres. The A shaped area of healthy 
fibres between the two areas of sclerosis are partly descending 
endogenous fibres, for fibres can be seen passing obliquely from 
the cornu commissural zone into this area, forming below the 
comma shaped tract. A good number of the fibres may, however, 
represent long fibres from roots of the lowest dorsal and upper 
lumbar, seeing that the clinical signs and microscopical exam¬ 
ination showed these roots were not much affected. In the 
lumbo-sacral region there is much shrinking of the posterior 
columns ; the only fibres that exist are the endogenous occupy¬ 
ing the cornu-commissural zone, oval area, septo-marginal and 
Gombault’s triangle, but the fibres in these tracts appear very 
much diminished. The fibres which are most atrophied are those 
forming Goll’s column (long fibres), cerebral, and those concerned 
with reflex spinal tonus, viz., those occupying Charcot’s root zone. 
These two sets of fibres seem very completely atrophied. The 
fibres which enter the column of Clarke as soon as it appears at 
the level of the second lumbar segment, are not completely 
destroyed; some fibres can still be seen entering the column 
at different levels, and breaking up into a plexus around the 
cells; still there is very considerable atrophy of this plexus 
(examination of the photomicrographs of Plate III. will enable 
the reader to follow the above description of the changes in the 
spinal cord). Lissauer’s tract is not so markedly atrophied even 
in the lumbo-sacral region. This may account for the fact that 
the cutaneous sensory disturbances were in proportion to the 
marked ataxy and helplessness, but slight comparatively. The 
slow progress of the disease may be connected with the blindness 
from optic atrophy. Examination by Nissl’s method showed that 

Fourth Cervical, 

Eighth Cervical, 

Tenth Dorsal. 

Fifth Lumbar. 

Tabes in Asylum and Hospital Practice. 

To face p. 126. 


■ ii in iiia •-.rasaac-. jcet 




the spinal motor cells were normal in appearance, the granules of 
Nissl were normal in the cytoplasm and on the processes. This 
agrees with the fact that there was not very marked hyptonus, 
and the muscles were of good colour and in no degree wasted. 
There was an abundance of small association and sensory cells of 
normal appearance in the anterior and posterior horns. 

Case 29.— Advanced tabes (which commenced with gastric crises at 
17?), ataxy and double vision at 28. At 39 admitted to 
asylum for an attack of mania with visual hallucinations and 

A. R., aged 39, general servant. No history or signs of 
specific disease. She says she had rheumatic fever at 17 (?) No 
history of ulcers on the eyes. Just after age of 17 she had attacks 
of vomiting, which would come on without any food in the 
stomach. Mother died of consumption ; father of senile decay; 
nine brothers and sisters, of whom seven are alive. At the 
age of 26 she commenced to have shooting pains in the legs. 
Could not walk about in the dusk without tottering, and used to 
totter when she washed her face. At 29 she had double vision, 
and saw Mr. Nettleship, at Moorfields. He said that there was 
loss of sense of position in the feet; she was taken into 
St. Thomas's Hospital under his care. She had drooping of the 
right eye, and was treated with blisters round the forehead. She 
went out and took a situation, but found that her right leg used 
to give way from time to time; she still had gastric crises ; 
.gradually walking became more difficult, and a stamping gait 
developed. She went into Highgate Infirmary incapacitated; 
.gradually legs became more helpless, and the vomiting became 
very severe. The vomiting has ceased for the last two years, but 
sbe still has the girdle and lightning pains, but not nearly so bad* 
.as before. She has not full control over the bladder, fairly good 
oontrol over the bowels, but cannot wait for either micturition or 
defaecation. She had been suffering from irregular catamenia, 
which sometimes was suppressed for a year; this came on before 
the diplopia. Had complete loss of power in the legs for six 
years. Prior to this there were spontaneous unconscious irreg¬ 
ular jerky movements when she was in bed. She also had 
irregular jerky movements in the hand, in attacks resembling St. 
Vitus’ dance. Had pins and needles in the fingers (paraesthesia). 

In August, 1899, she suddenly lost herself, and developed a 
shakiness in the hands ; she spilt her food owing to choreiform 
spasm. She lost consciousness, and had visual hallucinations. 



She thought she saw the matron making preparations to burn her 
up, and this became a fixed idea for a short time. She did not 
remember her relatives when they came to see her. Delusions 
that she was being tried by a judge and jury for some supposed 
crime. She had the delusion that her brother had been killed in 
trying to assist her. She was transferred to an asylum at the end 
of October. When, however, she was admitted to Colney Hatch, 
there was but little mental affection. The nurse says she has had 
no delusions or hallucinations. She now seemed very intelli¬ 
gent, and gives a most intelligent history of her illness. 

Condition on admission .—Loss of sense of position in both 
hands. Cannot touch nose with fingers when the eyes are shut. 
No affection of speech ; hearing normal. Legs extended in bed, 
feet inverted and flexed at the ankle, the knees extended. 
Complete paralysis of the feet and legs; she is unable to move 
any of the joints of the foot or leg, and cannot move her hips. 
There is marked foot drop and inversion of the feet. Knee-jerks 
absent on both sides ; the muscles are wasted, but how far this 
is due to prolonged disuse I cannot say. Plantar reflexes gone, 
epigastric reflexes brisk. Great weakness in muscles of back and 
neck, causing a certain amount of lordosis. She has to jerk her 
head to get it erect. All the muscles respond normally to the 
faradic current. No tenderness on percussion over her spine. 
Eight disc indistinct, and smaller than natural. Pupils, 6 mm., 
react to accommodation, but not to light. The sensory charts 
made in this case exhibited very marked cutaneous sensory 
disturbances to touch, pain, and heat and cold, in the regions 
supplied by the roots of the third to the tenth thoracic, and from 
the fourth lumbar to the last coccygeal. There is delay and 
diminution of cutaneous sensibility of a partial character in the 
areas supplied by intervening roots, and above the complete 
anaesthesia of the trunk there is hypaesthesia of the skin of the 
arms and of the trunk as high as the second intercostal. All the 
roots, therefore, below the third or fourth cervical are affected, 
and one would expect to find complete denudation of fibres in 
the roots, corresponding to the areas of complete anaesthesia, 
accounting in a measure for the complete loss of power in the 
lower extremities. 

Case 30.— Tabes , married woman , syphilitic history , mental crises 
in the form of hallucinations and delusions , Charcot's joint , 
gastric crises , preceded by pains in the swollen knee-joint . 

E. C., aged 39, married woman admitted to Banstead, August, 
1898, with acute mania, hallucinations and delusions. There was 



a history of six miscarriages and no children, but no history of 
insanity or nervous disease in the family. There are scars of old 
syphilitic ulcers on the legs. The symptoms of tabes commenced 
at the age of 33 with lightning pains, for which she attended St. 
Thomas’s Hospital. When she was 36 years of age she fell down 
stairs, her right knee swelled up, and she was delirious . She was 
taken to St. Thomas’s Hospital, but was a week later transferred 
to the Lambeth Infirmary on account of hallucinations and 
delusions. “ Men with monkey’s skins came and stole her things 
out of the drawers.” It was real to her then, but she now knows 
it was only a delusion. Once only while she has been at Ban- 
stead (two years), has she had any real mental disturbance. She 
was, according to the nurse, delirious and had visual hallucina¬ 
tions : she saw her husband and friends at her bedside, and wanted 
to get out of bed and go with them. She suffers with severe 
attacks of gastric crises at times, which last for several days. The 
crises seem to be preceded by pains in the right swollen and 
diseased knee-joint. Over the external and internal condyles 
there is a sinus, from which pus is constantly discharging. The 
joint is nearly 20 ins. in circumference and disorganised. The 
muscles of the leg are greatly wasted, and there is well marked 
foot drop. The patient states very definitely that during the gas¬ 
tric crises lightning pains radiate all over the body, passing down 
the legs and arms, up the back, and terminating in the forehead, 
but never .spreading to the face. The knee-jerk in the left leg is 
absent; there is hypotonus of the hamstring muscles, and a 
marked loss of joint sensibility in the lower limbs. Argyll- 
Robertson pupils. There is no loss of tactile or painful sensibility 
inf the upper limbs, but slight incoordination and loss of sense of 
position. Painful and light tactile sensation is lost or impaired 
below the knee, and there is slight blunting or loss of light tactile 
sensibility in the area corresponding to the sixth, seventh and 
eighth segments. There is no bladder or rectal trouble. The 
patient was sent to St. Bartholomew’s, and the right leg amputated 
above the diseased joint, which was sent to me for examination, 
by the kindness of Dr. Claye Shaw and Mr. Walsham. 

Examination of the nerves of this joint showed atrophic 
degeneration somewhat similar to that which is found in the 
posterior root of an ataxic case, viz., disappearance of myelin 
from sheath, proliferation of nuclei of primitive sheath. This, of 
course, may be simply a disuse atrophy associated with prolonged 
immobility, or it might be explained by damage of the nerves 
from the dead bone and discharging sinus. 




Fig. 19. 

Teased nerve-fibres entering the peroneus longus muscle away from any 
obvious septic inflammation. At (a) the myelin is shown filling the neuri¬ 
lemma ; it has an opaque dull appearance, indicating a congulation neurosis. 
At those portions of the fibre where the myelin has disappeared the nuclei 
have undergone proliferation; ( b) is a fibre in which the myelin has quite 
disappeared. Staining, alum hsematoxylin, mounted in ammonium picrate 
and glycerine. Magnification 460 diameters. 

GROUP 3.—Tabo-Paralysis. 

Case 31. — Onset with fits , headache , loss of memory , insomnia; 
admitted to asylum with symptoms of acute mania and 
physical signs of tabes . Subsidence of mania , marked ataxy , 
convulsive seizures , gastric crises , shooting pains with associated 
delusions , lucid intervals , but a progressive mental enfeeble - 
ment . Death . 

I. D., female, aged 31, single. Occupation, colour printer. 
Admitted to Cane Hill on October 2,1897. 



History .—No family history of insanity or phthisis. She 
attended a dispensary about seven months for some disease of the 
genito-urinary organs, but whether this was syphilis cannot be 
definitely ascertained. She had two fits five months ago, and for 
the last three months she has had headache, loss of sleep, and 
failure of memory. Quite recently her speech changed, and she 
became very restless and talked incessantly. The cause of the 
attack is stated to be disappointment in love. 

On admission .—A young woman, thin and badly nourished, 
but with no signs of organic disease of viscera. Tongue clean, 
pupils equal and contracted. No reaction to light or accommoda¬ 
tion. Knee-jerks absent. She has general movement of head 
and arms. Waves her arms continually and moves her head 
about in ail directions. The movements of her arms are purpose¬ 
ful. She undoes her hair and does it up again continually, and 
keeps unbuttoning her dress. Her gait is unsteady and ataxic. 
She is destructive and very mischievous. Is wet and dirty in her 
habits. Will not keep in bed, but rolls off on to the floor. Men¬ 
tally she is in a condition of acute mania. Is very restless and 
resistive to everything. Unable to answer the simplest questions 
properly, but rambles off irrelevantly. Childish and foolish. 
Memory bad. 

November 2.—Symptoms of mania persist; she has required 
sedatives (such as chloral and paraldehyde) on account of her 
extreme restlessness. Still wet and dirty and very destructive. 

December 1, 1897.—She has become much clearer mentally. 
The attack of mania has subsided. She is fatter and stronger, and 
the movements have entirely ceased. She now has well-marked 
signs of tabes dorsalis. Ataxic gait and loss of knee-jerks. Pin¬ 
point pupils, slight reaction to accommodation, but not to light. 
Has anaesthesia of the ring and little fingers on both sides. 

January 2, 1898.—She has lately been having attacks of 
vomiting, and has complained of pains in her abdomen and legs. 
Is very shaky and ataxic, and is becoming very feeble. To-day, 
she had a convulsive seizure, and became comatose for sometime. 
Her face has lately become greasy and expressionless. 

March 1, 1898.—She has been practically bedridden since last 
note. Quite helpless and feeble, and has become wet and dirty 
in her habits again. Often vomits and complains of pain round 
' her waist. Her speech is now slurred, and her tongue tremulous, 
and she is more demented. Her condition now differs in no way 
from the last stage of general paralysis. 

April 14, 1898.—Still bed-ridden and extremely feeble and 



helpless. Has become very rigid in muscles of neck and limbs. 
Is quite demented and cannot understand or answer the simplest 
questions. Has paresis of left internal rectus. Occasional 
pyrexia. Her right pupil is now slightly larger than the left, but 
there is no reaction to light. 

May 18, 1898.—Still in bed. General rigidity of muscles all 
over body. Wet continually. No vomiting now. She improved 
in mental condition, and was able to get up and sew a little, and 
take a fairly bright and intelligent interest in her surroundings; 
but in the middle of July, she became very restless and excited, 
refusing to stay in bed because she said mice ran over her body 
and pillow. She makes frequent attempts to catch them. 
Continual use of sedatives necessary on account of her restless- 
condition. She complains of the treatment by the nurses, that 
they had put something chopped up in her milk, that they 
had scraped her bowels out and spoiled her features. This 
was no doubt an insane interpretation of the gastric crises. 
(F. W. M.). 

August 12,1898 (F. W. M.).—The patient says she is feeling 
much better. The nurse says she is quiet now, but she has 
been very excited and troublesome. There is typical ataxy of 
the lower limbs. The knee-jerks are absent and she is unable to 
stand or walk alone. When supported by two nurses she can 
stand with difficulty, but on closing the eyes she would fall if not 
supported. She can touch the tip of her nose with her finger, 
and she can write her name, but there is a good deal of fine 
tremor in the strokes. She complains of sharp shooting pains in 
the legs and round the stomach. She passes water involuntarily, 
but has control over the bowels. She has not menstruated since 
she has been in the asylum. She has lately had an ulcer on the 
cornea. Pupils, Argyll-Robertson, small, equal. There are no 
synaechise, and the fundi are normal. She complains of a feeling 
like wool on the soles of her feet, and she is unable to say what 
is being done to her great toe when it is flexed or extended. 
There is some loss of painful and tactile sensibility in the lower 
limbs. There is no tremor of the face or tongue. There is slight 
ptosis of the right eye-lid. Smell and taste are good, also hear¬ 
ing. Speech normal. 

Mental condition .—She appears to me quite rational, but her 
memory is somewhat defective. She told the nurse that she had 
a baby at Liverpool, and that she has had two abortions. She 
tells me the same story, and that she has lived with several men. 
Some time ago she had delusions that there were mice in the bed. 
When I last saw her she was in an unconscious state, and I 



judged that she was suffering from a congestive seizure of general 
paralysis. (F. W. M.) 

June 19, 1899.—Mentally the patient has greatly improved 
since I last saw her. She talks quite rationally, has no loss of 
knowledge of time or place, her speech is unaffected. She tells 
me that she has had many attacks of vomiting lately, and 
diarrhoea. She complains also of a tight feeling in her left side 
(gastric crises). She also tells me that she has a feeling of wool 
on the soles of her feet. There is considerable blunting of sensa¬ 
tion in the lower extremities, especially on the left side. She 
feels sharp pricking, but there is considerable delay, and blunting 
of sensation. There is no incoordination in the hands now. She 
can knit and sew. Complains of dimness of vision in the left eye. 

October, 1899.—The patient has been free from mental symp¬ 
toms for the last six months, and she talks in a perfectly rational 
manner, without any hesitation or slurring of speech. She com¬ 
plains of a girdle sensation round the waist, and for the last three 
months she has suffered from severe attacks of vomiting and 
nausea. She has had shooting pains in the legs, is constipated, 
and wets the bed at night; she has had no more fits. There is 
considerable incoordination in the hands, and she is unable to 
sew as well as when I last saw her; she has numbness of the 
ring and little fingers of the left hand. 

October 9, 1900.—Patient is in a fairly rational condition of 
mind, and able to answer questions. She knew me quite well. 
She has had many* attacks of vomiting since I saw her, with 
shooting pains in the left side and legs. She has attacks of pain 
in her legs nearly every day. The attendant informs me that not 
long ago she became very restless and violent, and very difficult 
to manage. She believed that she was going to marry Dr. B., 
and wrote numerous letters on the subject asking him to provide 
clothing for her. She tried to tear out all her gray hairs, and 
wished to have all her teeth drawn in order that she might be 
made beautiful and captivate the doctor. She was very destruc¬ 
tive, tearing up her clothes. She remained in this maniacal state 
for over a month. When she had fits she would lose con¬ 
sciousness, sometimes for four hours together; the convulsions 
were mostly on the left side. 

Physical examination .—The limbs are well nourished, but 
there is very marked hypotonus in the hamstring muscles. The 
extended limbs can be bent to an angle of 75° with the body. 
There is loss of sense of position in the hands. Sensation, tactile, 
absent in the shaded parts of the diagram, although there are 



scattered patches of normal sensation with a delay in response, 
tested by lightly touching with the finger. Painful sensation, 
pricking with a needle; result shown in the accompanying 
diagram, likewise thermal sensation. In parks of the body 
other than those indicated in the diagram she always gave a 
correct answer, showing that she was able to appreciate and 
respond to the stimulus. 

July, 1901.—Smell and taste.—She cannot smell peppermint, 
assafcetida, or rose-water. She can taste quinine, but syrup and 
acids are not appreciated. Hearing.—Hears a watch 18 inches 

on either side. Colour vision.—Picks up correctly colours with 
one eye closed, but marked incoordination and failure of judg¬ 
ment of distance noticed. Pupils.—Eight 3 mm., left 2| mm.; 
inactive to light, very sluggish to accommodation, outline irre¬ 
gular. She takes her food, but is much weaker than she was; 
she has had no fits lately and no sickness. Tongue and lips 
tremulous, but the speech is not affected. She has no control 



over the sphincters, and when she wets the bed she says that 
some one else has done it. Although so emaciated, she has a 
ravenous appetite. After she has eaten her dinner, she fancies 
that some one else has had it, and she will steal another patient’s 
dinner if she is not looked after. She is quarrelsome, and will 
smack the faces of patients who sit next to her. She forgets the 
incident the next minute. She forgets the names of people, but 
she has not personal illusions. She has not complained of bad 
tastes in the mouth or bad smells, nor has she now any delusions 

Fig. 21. 

— Thermo-anaesthesia 

of poisoning. She recognised her friends, but her knowledge of 
time and place are extremely defective. She does not know 
whether it is winter or summer, morning or afternoon. I told 
her that she had had her dinner, she then replied that it must be 

January, 1902.—Death from pneumonia. 

Autopsy .—Broncho-pneumonia affecting the right lung espe¬ 
cially. Nothing especially noteworthy in the other organs, except 



the ovaries; the left Fallopian tube is matted to the ovary and 
uterus, and exhibits the appearance of old non-tubercular sal¬ 
pingitis. There were no signs of syphilis on the body, but the 
vagina was large, and this, together with the absence of hymen, 
a scar on the cervix and the condition of the Fallopian tube 
mentioned, accords well with her statement of abortions and the 
history of some venereal infection. Brain .—No adhesions of the 
dura mater, slight excess of sub-arachnoid fluid, slight thickening 

and opalescence of pia-arachnoid over the frontal and central 
convolutions. Some adhesions along mesial surface of frontal 
lobes, very little wasting or thickening of membranes of pre-frontal 
or orbital lobes. Some wasting of first, second, and third frontal 
at junction with anterior frontal; no obvious wasting of Broca’s 
convolution ; optic nerves small, but not gray. Olfactory nerves 
small, membranes thickened, opalescent, and adherent about the 
tip of the temporal lobes and origin of olfactory. Granulation of 



lateral ventricles, but very little dilatation. Marked granulation 
and some dilatation of the fourth ventricle ; erosions of central 
convolutions on stripping the membranes, decided atrophy of 
upper two-thirds of central convolutions on both sides. Naked 
eye atrophy and gray degeneration of the posterior roots and 
posterior columns of the spinal cord. 

Microscopical examination .—Teased preparations of posterior 
roots exhibited a large number of empty sheaths with proliferated 
neurilemmal cells; others, the myelin sheath partially gone, or 
irregularly disposed—indicating a regressive atrophy. There are 
comparatively few healthy medullated fibres to be found in the 
posterior roots of the regions of the cord, where there is usually 

The degeneration of the spinal cord was the same in character 
as met with in ordinary tabes ; its distribution is shown in the 
accompanying chart, to which attention is called, as to the follow¬ 
ing facts. There is a very complete degeneration of the posterior 
roots in the upper nine dorsal segments, and a corresponding 
extensive degeneration in the postero-external columns ; it will be 
observed that at the fifth dorsal segment, there is a marked atrophy 
-of the posterior horn, and an indentation in this region on one side. 
In the lumbo-sacral region there is also complete degeneration of 
the posterior roots, and the roots of the cauda equina. Although 
the endogenous systems do not present the same degree of de¬ 
generation as the exogenous, it will nevertheless be observed that 
the chart indicates, especially in the dorsal and lumbo-sacral 
regions, a considerable destruction of the fibres arising from the 
cordonal cells, and no doubt this fact indicates more advanced 
Regeneration, and explains the marked ataxy of the lower limbs 
from the very commencement and the only slight incoordination 
of the upper limbs, for the case shows that she was able to knit 
and sew. 

The distribution of the degeneration accords fairly well with 
the chart (fig. 23), indicating the distribution of anaesthesia and 
-analgesia observed during life, six months before she died. Pro¬ 
bably the roots on the right side were subsequently affected, for 
the roots in the dorsal, lower lumbar and sacral regions were 
practically denuded of fibres on both sides. 

The whole cord was not larger than that of a child of two 
years, particularly is this noticeable in the dorsal region. Another 
fact indicating a metabolic change was the difficulty with which 
the myelin sheaths of the nerves stained, resembling in this 
respect the cords of new born children. Owing to the extreme 
atrophy of the posterior roots, therefore, of the projections in the 



Fig. 23. 

Diagram made with Edinger’s projection apparatus, from sections of the spinal 
cord stained by Weigert-Pal method. Complete degeneration and atrophy of fibres is. 
indicated black, partial atrophy by black dots. 



cord, the course of endogenous fibres still existent could easily be 
followed and the following notes were made {vide fig. 24):— 

Cauda equina .—Complete degeneration of all the fibres of the 
posterior roots, with imperfect staining of fibres of anterior roots. 
A section of the fourth sacral segment roots included showed a 
small triangle of fibres in the posterior column, endogenous, and 
corresponding to the posterior median triangle of Gombault and 
Philippe. This tract of fibres is continuous with a tract which 
lies along the median fissure in the first, second, and third sacral 
segments; at the fifth lumbar segment, there are no root-fibres, 
and these septo-marginal fibres can be traced along the posterior 
column to the posterior horn, while other fibres can be traced from 
the cornu commissural zone to the base of the posterior horn. The 
septo-marginal tract is seen to be continuous with the oval area of 
Flechsig, so that we may consider these three tracts with separate 
names are merely divisions of the same system of endogenous 
fibres. At the level of the first lumbar and last dorsal, at the 
very extremity of the posterior median fissure, there exists a 
small triangle containing still a number of undegenerated fibres. 
This tract of fibres is continuous below with the oval area, 
of Flechsig, and above with the internal zone, which consists 
in a great measure of descending endogenous fibres; it is 
is continuous above in the upper dorsal region with the 
comma shaped tract. Study of the sections shows that a large 
number of reflex collaterals are given off by these endogenous 
systems and that they consist of two sets of fibres, ascending and 
descending . The comma tract, posterior internal triangle, fibres 
continuous from, there along to the median fissure which form 
the septo-marginal tract, oval area of Flechsig and the posterior 
triangle of Philippe constitute the latter. Collaterals are given off 
all the way down in two situations: (1) in the substantia gela- 
tinosa, where the fine fibres of Lissauer’s zone end ; (2) in the 
posterior horn opposite the root zone. The ascending endogenous 
system forms the cornu commissural zone of Westphal; the fibres 
from this zone in the dorsal region can be seen very distinctly 
running forwards in three groups of fibres: (a) External to 
Clarke’s column; ( b) Internal to Clarke’s column, to form a 
plexus at the junction of the anterior and posterior horns; 
(c) Fibres decussating in the posterior commissure from the 
other side {vide fig. 27). These fibres can be distinctly traced, 
owing to the complete atrophy of the collaterals of the exogenous 
fibres around the cells of Clarke’s column; the fibres from the 
latter entering the direct cerebellar tract can also be seen dis¬ 
tinctly as they pass outwards and upwards across the base of 



Fig. 24. 

Outline drawing of 
spinal segments, show¬ 
ing fibres of endogen¬ 
ous origin remaining 
in posterior columns 
of spinal cord at levels 
where there was 
complete degenerative 
atrophy of the roots 
2 D, 4 D, 6 D, and 
those intervening; 
also nearly complete 
atrophy at lower levels 
in the dorsal region. 
The fibres form the 
comma tract of Max 
Schultze. They give 
off collaterals at 
different levels to the 
gray matter of the 
posterior horn, some 
of which decussate in 
the posterior commis¬ 
sure. They probably 
keep entering and 
leaving the white 
matter at different 
levels. At various 
levels they pass back¬ 
wards to enter into 
the formation of the 
posterior internal tri¬ 
angle. At the first 
lumbar they leave this 
position to form the 
septo-marginal tract. 




the column. Although these endogenous fibres can be distinctly 
seen owing to the complete atrophy of the exogenous systems, 
yet, as the chart shows there is a great outfall of these fibres in 
the whole of the dorsal and lumbo-sacral regions, the descending 
system being more affected than the ascending. Briefly, the 
degeneration corresponds with the advanced second stage or com¬ 
mencing third stage of ataxy, and the marked atrophy of roots in 
the upper dorsal and lumbo-sacral regions corresponds with the 
anaesthesia and analgesia observed during life, more marked on 
one side than the other. 

The degeneration of roots and posterior columns in the eighth 
cervical and first dorsal, more marked on one side than the other, 
corresponds with the more marked sensory disturbance (observed 
during life) on the left than the right side. 

The fact of the existence of the gastric crises may be associated 
with the marked degeneration of the roots in the mid dorsal 
region, and especially with the obvious affection of the gray 
matter in the fifth and sixth segments. It will be observed that 
there was no direct or crossed pyramidal degeneration, except 
possibly in the lowest lumbar and sacral regions, and this would 
accord with the fact that there was little chromophilous change 
in the Betts’ cells of the cerebral cortex. 

Brain .—Examination by cell and fibre methods. There is 
very little vascular change in the cortex as a rule, but typical 
plasma cells were found around the vessels in the orbital 
region; also excess of lymphocytes and endothelial cell proli¬ 
feration ; there .is proliferation of the glia cells, but not many 
spider cells are seen. Sections of the parietal lobule, ascend¬ 
ing frontal, ascending parietal, pre-frontal, orbital and angular 
gyri were made, stained by Nissl’s method and examined. In 
all these regions the cells of the molecular layer of Cajal, the 
small and medium sized pyramids were found diminished in 
numbers, distorted in shape, not arranged as a rule in columns, 
their processes are broken off, and the bodies of the cells present 
various atrophic and degenerative changes of varying degrees of 
intensity, although some of the cells exhibit a fairly normal 
appearance. The cellular changes were more marked in the pre¬ 
frontal and frontal regions than elsewhere. These changes appear 
to be of the nature of a primary cell atrophy. The Betts’ cells in 
the ascending frontal are in groups, and some cells of a group 
appear fairly normal, while others show chromolytic changes, 
eccentric nucleus, and breaking off of the processes, indicative of 
an acute change. 



Examination of the same regions by the Weigert method 
showed corresponding atrophy and partial disappearance of the 
tangential, supraradial and interradial fibres most marked in the 
regions where the cell atrophy was most apparent. 

Case 32 .—Early ataxic general paralysis in a young married 
woman, the subject of syphilis (acquired before marriage, in all 
probability). Death in less than a month after admission from 
pneumonia. Deft knee-jerk absent , right-sided fits, speech 
affection , right hemisphere weighed 20 grammes more than left. 

H. W., aged 26 years, admitted to Ciaybury, June 21, 1901. 

History (from husband).—No family history of insanity, 
patient’s brothers and sisters all strong and healthy. Married 
seven years ago at the age of 19, and before marriage she was an 
upholsterer by trade. Husband states that occasionally she has 
been drunk, but he is sure that her illness was not due to drink. 
She was an attractive-looking, good, and affectionate wife, and 
came from a very steady, good-living family. The husband 
attributes her illness to an accident she met with while with 
child; this child was still-born with difficult labour. Sub¬ 
sequently she had five or six miscarriages, but no children. For 
six months, or possibly longer, as she hid it from her husband, 
she suffered with a bad leg. Patient was the second wife of 
Mr. W., and in about September last he lost his daughter, aged 
10, a child of his first wife, and the combined worry, husband 
thinks, constituted the exciting cause of the patient’s illness. He 
denies that he ever had venereal disease, and I judged after the 
interview with him that his wife had been infected before having 
relations with him. Patient never complained of pains in her 
legs, except from the ulcer. As her illness progressed she had 
visual hallucinations of policemen coming into the house; she 
also had delusions that each person she met was a policeman, and 
that he was coming to lock her husband up. For the last eight 
or nine weeks husband has noticed that her speech has been 
affected. She had two or three fits before admission, the mouth 
being drawn to the left side, following the fit, but afterwards it 
came to the normal position. 

Condition on admission: Mental .—Rambling and incoherent 
in her speech, believes that she has not been out of her house for 
five to seven years. Physical .—The right pupil larger than the 
left, both fixed ; the right knee-jerk present, the left absent. She 
was suffering with palmar psoriasis and a syphilitic ulcer of the 
right leg, with the usual characteristic brown pigmentation 



around. The teeth were worn down, otherwise her conditon 
was good, yet she was unable to walk. Her speech and 
expression were characteristic of general paralysis. The memory 
was very much impaired, and she was dull and sluggish in answer¬ 
ing questions, and she had no knowledge of time or place. When 
questioned she jumps up as if to attention, but cannot maintain 
herself in the standing position. 

Died July 7, 1901. 

Post mortem .—Body well nourished, physique good, muscular 
system developed, post-mortem rigidity just commencing. On the 
Tight leg there is an old ulcer 1 in. by 2 ins., with pigmentation all 
round, the extent being as great as could be covered by the hand, 
typically syphilitic. The pupils were irregular, but equal, both 
being 5 mm. in diameter. There was no obvious thickening of 
the pia-arachnoid, but sub-pial haemorrhages over the frontal 
region; it was adherent along the mesial surface of the frontal 
lobes. Weight of encephalon 1,120 grammes, appearance normal, 
with the exception of the haemorrhage referred to. Weight of 
right hemisphere 490 grammes, weight of left 470 grammes, 
weight of cerebellum and pons 160 grammes. There is some 
apparent wasting of gray matter n the pre-frontal regions of both 
hemispheres. The ventricles were not granular or dilated. The 
lateral sacs of the fourth ventricle were slightly granular. 

Right lung, weight 450 grammes, lower lobe in a state of 
commencing red hepatisation, commencing pneumonia of upper. 
Left lung, weight 650, lower lobe semi-solid, sinks in water, in a 
state of red hepatisation, commencing pneumonia of upper lobe. 

Heart and valves all healthy, no atheroma aorta. Liver 
rather pale and fatty, spleen softer than normal, kidneys pale, 
otherwise normal. Stomach, pancreas, &c., normal, intestines 
normal. Os uteri dilated, tough and fibrous, cyst in left ovary 
the size of a pigeon’s egg. 

Cause of death , immediate .—Double pneumonia. 

Other pathological conditions .—Very early general paralysis. 

General summary .—Had she not contracted pneumonia a week 
or two after admission, she might have lived several years, as her 
general condition was excellent. 

Case 33.— Tabetic general paralysis in which the mental symptoms 
preceded the cord symptoms . Death ivithin three months of 
admission. Characteristic brain and cord lesions. 

E. A., aged 32, married, policeman ; late Army Service Corps, 
admitted to Hanwell, October 26, 1899, suffering from symptoms 
of general paralysis (tabetic form). 




Family history (obtained from wife).—He is one of a family 
of eight, all alive and healthy, father and mother both healthy, 
no history of insanity or other neurosis, no history of phthisis. 

Personal history .—Informant has been married to him for 
ten years ; as far as she knows he was always bright, happy, and 
healthy as a young man ; was a good husband and father; was in 
the army for ten years before marriage; they have had four 
children, eldest 8, youngest 2, one child died, aged 2£ of pneu¬ 
monia. Wife has had no miscarriages, and no history of syphilis 
can be obtained from her. She has seen him occasionally the 
worse for drink, but denies that he was habitually a heavy 
drinker. After the death of his child eighteen months ago, she 
first noticed that he became absent-minded, forgetful and 
melancholy, and he was obliged to leave the police force. His 
speech was first affected about two months ago; he has had no 
fits as far as she knows; his gait has become affected since his 
admission to the Infirmary three weeks ago. 

He has a scar on glans penis, and two large scars in right 
groin, shotty glands in both groins; in spite of the above evidence, 
he denied having had venereal disease. 

Physical condition .—Body somewhat emaciated, heart and 
lungs free from any symptoms of disease, tongue clean, tremulous, 
protruded slightly to the right, gait staggering, marked inco¬ 
ordination of muscles of locomotion and inability to walk without 
support. The unsteadiness is increased with the eyes closed and 
there is some difficulty apparent in touching the tip of his nose. 
The knee-jerks are absent, and there is some hypotonus of the 
hamstring muscles. The pupils are small, the right a little larger 
than the left and give no response to light ; accommodation 
active. Speech most inarticulate and slurred, making it difficult 
to understand what he says. There is marked tremor of the 
lips and tongue. Slight drooping of both eyelids. He com¬ 
plains of rheumatic pains in his legs. No loss of sensation was 
observed on testing him by pricking and touch. 

Mental state .—Confusion of ideas, impairment of memory, and 
mild delusions that he has money in the bank. He is restless 
and sleepless. 

November 30.—Paresis rapidly progressing, has lost control 
over his sphincters, but asks to be changed and cleaned ; he is 
rapidly emaciating. 

December 11.—Commenced having epileptiform seizures, and 
he died on December 13 from acute pneumonia. 

The brain showed the macroscopic signs of early general 



paralysis ; the pia-arachnoid was slightly thickened and adherent 
over the fronto-central convolutions, erosions occurred on 
stripping, the gray matter was diminished, striae indistinct. All 
the ventricles were somewhat dilated and granular. The spinal 
cord presented no naked eye change, but microscopical examina¬ 
tion revealed early tabetic atrophy, as the subjoined micro¬ 
scopical examination shows :— 

Fifth lumbar.—Slight diffuse sclerosis of posterior columns, 
except in the cornu commissural zone and the oval area. Slight 
diffuse sclerosis of crossed pyramidal tracts. Eighth dorsal.— 
Slight diffuse degeneration in posterior median column. Well- 
marked sclerosis of cornu radicular zone. Second dorsal.—Ditto 
Seventh cervical.—Slight degeneration of posterior median, better 
marked degeneration of band just outside this, coming, doubtless, 
from eighth cervical, first and second dorsal-fibres. At the base 
this spreads out to reach the posterior horn. 

In no part of the cord were the endogenous fibres of the 
posterior columns obviously degenerated. The posterior roots 
show atrophy and denudation of fibres, especially in those regions 
where the posterior column degeneration is marked. The vessels 
and membranes show little or no change, and the cord presents 
little change in size or shape, for there is comparatively little 

Case 34.— Ataxy and slight early seizures and symptoms of general 
paralysis , abeyance of ataxic symptoms } pronounced mental 
symptoms following seizures. 

F. J., compositor, aged 49. Admitted to Colney Hatch. My 
attention was called to him by Dr. Seward on account of his 
ataxic walk. He gave a history of syphilis, scar on penis, and 
from his own account he had evidently lived a very rackety life. 
There was no history of insanity in the family. When I first saw 
him he was not much affected mentally, but he was ataxic; he 
had pains in the legs, unsteadiness in his gait, which was increased 
on closing his eyes. The pupils were equal, contracted to 3 mm. 
and did not respond to light, but sluggishly to accommodation. 
The knee-jerks were absent, and there was hypotonus in the 
limbs. The speech was hesitant and somewhat syllabic, and the 
tongue tremulous. Six months later when I saw him he was a 
most pronounced general paralytic ; he had had seizures, and the 
speech was characteristic of advanced general paralysis. He had 
delusions of wealth, grandeur, and strength, and a markedly 




exalted expression (vide photo). His walk was now a shuffle, 
hut he could stand without any swaying with his eyes shut. The 
knee-jerks are still absent, but there is no hypotonus in the limbs. 
He subsequently died. The brain presented all the characteristic 
appearances of general paralysis. The spinal cord was forwarded 
to me for examination with the following results : — 

Fig. 25. 

The photograph illustrates a condition of marked exaltation and grandiose 
delirium ; at the time this was taken the patient was telling me that his 
brain was geared up to 990,000. 

Microscopical examination .—The sclerosis, although most 
obvious in the exogenous systems of the posterior columns, is not 
limited thereto, as there is a very definite sclerosis in the comma 
tract, but the cornu commisural zone of Westphal in the lower 
dorsal and lumbo-sacral regions is intact. There is diffuse scle¬ 
rosis of Goll’s column in the cervical region and a well-marked 



band of sclerosis corresponding to 
roots supplying the upper limb. 
There is well - marked atrophy 
and denudation of fibres in the 
middle third of the postero-exter- 
nal column corresponding to Char¬ 
cot's root zone in the dorsal and 
lumbo-sacral regions, with atrophy 
and disappearance of many of the 
fibres of the plexus around the 
cells of Clarke's column. This 
atrophy is most apparent where 
Clarke’s column is most developed 
—viz., in the lower dorsal and 
the upper lumbar regions. 

The median oval area of Flech- 
sig, and Gombault and Phillipe's 
posterior triangle appear to be 
only slightly denuded of fibres. 
There is some acute degeneration 
of the crossed pyramidal tracts on 
both sides throughout the cord, 
and a little degeneration in the 
direct tracts (vide chart). 

Case 35.— Tabes of two or three 
years' duration , very advanced 
in legs and arms . Gastric 
crises . Bladder and bowel 
troubles . Admitted to asylum 
suffering with mania , exalted 
notions , and intellectual con¬ 
fusion . 

Pig. 26 . 

N. A., admitted to Colney Hatch May, 1901, Russian Jew, 
aged 33, a tailor by occupation, has to do a great deal of walking, 
and always stands at his work as a cutter. He has been fifteen 
years in England, married nine years. After marriage, wife had 
four miscarriages, then three children died in early infancy, 
.finally two living. At 15 years of age the patient contracted 
a chancre, which was treated for two years, suffered with sore 
throat, rash, and falling out of hair. There is no scar visible; 
glands in the groip are enlarged. He is a temperate man, 
smokes; there is no history of insanity in the family. 



Physical condition .—He has a difficulty in standing and walk¬ 
ing, which he says commenced two years ago. He was treated at 
St. Mary’s Hospital twelve months ago for shooting pains in 
the legs, cord-like feeling round the waist, and loss of memory. 
He now walks with a jerky wide base, heels down first. He 
complains that occasionally his legs have given way under him. 
Eomberg symptom marked, knee-jerks absent, sense of position of 
joints lost, especially in legs, very marked hypotonus of hamstring 
muscles. Superficial reflexes exaggerated, pupils unequal, right 
2|mm., left l|mm., inactive to light, active to accommodation, 
says that he does not see well with the left eye. Complains of a 
frequent desire to micturate, and difficulty in passing water. He 
has trouble with his bowels and bad attacks of vomiting. His 
speech is syllabic and tremulous. Being asked to write his name 
and address, he held the pencil between the side of the middle 
finger and tip of index, and the writing, like the speech, was very 
ataxic, syllabic and tremulous. There was slight tremor of the lips 
and tongue noticed. 

Mental condition .—There is some mental confusion and inco¬ 
herence, and a moderate amount of exaltation. He thinks that 
he has £250 a year from the War Office, that he is a General in 
the 17th Lancers, but on questioning him, he knows nothing 
about the regiment. He is the owner of a diamond factory in 
Birmingham. There is a sub-stratum of truth in these delusions* 
With regard to the former statement, he probably makes uniforms 
for officers in the Army, and a good cutter, such as he may have 
been, would easily make £250 per annum. With regard to the 
second statement, like many other of these aliens, he has been in 
South Africa, and possibly in the illicit diamond trade. 

No doubt there is considerable disturbance in the sensibility of 
the skin, but the facts elicited on this occasion were not considered 
sufficiently reliable to be included in the notes. 

Case 36.— Tabo-paralysis , commencing with a fit , followed by 
transitory aphasia. Later typical signs and symptoms of 
ataxy , melancholia , attempted suicide , progressive degeneration 
of brain and cord , with delusions and illusions , death , with 
typical naked eye signs in the brain of general paralysis . 

A. H., aged 38, admitted to Hanwell, July 31, 1896, for 
melancholia and attempted suicide, which he nearly succeeded in 
accomplishing by cutting his throat, the scar of which is evident. 
Occupation, fireman on an engine, standing all the time, exposed 



to weather and the heat of the furnace. He attributes his ataxy 
to his occupation, and he is very depressed in consequence of his 
being unable to continue his work. 

Family history .—Maternal uncle died in an asylum. 

Personal history (from the wife).—She has known the patient 
for eleven years. During this time he has always been ailing. 
For the past five years he has been much worse. Five years ago 
he had a seizure of some kind, and lost power of speech for two 
days. Since that time his speech has become much worse. In 
1892 he found a difficulty in walking in the dark, and he had a 
velvet-like feeling on the soles of the feet. Twelve months ago 
he complained of a girdle sensation, followed by what were 
evidently rectal crises. Later on he suffered with loss of sexual 
power. His mind became affected after a severe fit which he had 
fourteen months ago. On the 1st of June last he had another fit, 
remaining unconscious for one hour. The medical certificate 
states that he is simple and childish, laughing insanely when 
spoken to. He had collected a lot of useless buttons, pebbles, 
bits of clay pipe, and attempted to explain the uses to which he 
would put them. His statements are rambling and contradictory. 
Twelve months ago he attempted suicide. 

Present state (August, 1896).—He has an expression of 
depression, but I could discover no delusions or mental affection 
beyond this extreme depression, due to his being in an asylum, 
and unable to maintain his wife and children. His knowledge of 
time and place are good, likewise his memory for recent and past 
events. There is no tremor in the tongue, or face muscles, nor is 
the speech obviously affected. There is no ocular paralysis, no 
signs of syphilis on the body, and no history of the disease, but 
the possibility cannot be absolutely excluded. He is temperate in 
habits. He has a marked ataxic 'gait, Argyll-Robertson pupils, 
absence of knee-jerks, loss of sense of position in lower limbs, 
not in upper; complete loss of power over rectum, partial over 
bladder, cutaneous anaesthesia could not be determined in a 
reliable manner, owing to his refusal to answer. 

November, 1897.—Patient suffered with severe epileptiform 
attacks, followed by delusions of persecution. People are putting 
dung in his food, and are playing upon him with electricity ; his 
gait is not so ataxic. 

August, 1898.—He is still suffering with delusions of poisoning, 
accompanied by great mental depression. He had been suffering 
with dysenteric diarrhoea, and he considers it was due to the 
medicines and food. 



April 27,1899.—The notes state that he has become paralysed 
on the left side of the body; he is still suffering with delusions 
of poisoning, and people playing upon him with electricity, and 
he is more demented. 

July 31, 1899.—Patient is certified as dying from dementia 
and paralysis. The post-mortem notes state that the brain 
weighed 46 ozs.; the convolutions on the right side were the seat 
of extensive atrophy and white softening in the ascending frontal, 
first temporal and angular gyri; wasting of the left leg is also 

Case 37.— Tabo-paralysis. Grandiose delusions , acute mania y 
macropsy y slight ataxy , pains attributed to electricity , auditory 
and visual hallucinations . Death eight months after onset of 
mental symptoms . 

N. E. E., aged 46, admitted to Hanwell, June 28, 1901; occu¬ 
pation woodcarver and turner. His work necessitated standing 
all day. 

, Personal history (from wife).—He has been worried lately a 
good deal by the foreman on account of his inability to perform 
the work satisfactorily. He has been married twice, but has no 
children. His first wife had one miscarriage. He has been 
married to his second wife sixteen years. Patient’s father died 
raving mad, was very intemperate, probably mania a potu , as the 
delirium was only a few days before death. An aunt was very 
eccentric, no history of phthisis. Patient when very young had 
fits between the ages of 4 and 6, but none since. He has been a 
steady, temperate man, thoroughly moral and very clever and 
industrious. The wife says that two doctors pronounced the 
opinion that the patient had syphilis when he was a young man, 
for which he was treated for some time. The patient himself, 
when questioned about this, said it was what is called a soft sore ; 
it was only treated locally. 

History of present illness (from wife).—Eight or nine years 
ago he suffered with dyspepsia and dilatation of the stomach. 
He has always been an excitable man, and his health has broken 
down latterly. He has complained of his eyesight, and he has 
had sharp shooting pains in the legs. The mental symptoms 
started about six months ago with extravagant ideas. 

Physical condition .—Gait not ataxic, but walks with a slightly 
wider base than usual, Romberg symptom is absent, muscles 
well developed and strong, knee-jerks absent, superficial reflexes 
exaggerated, some hypotonus of hamstrings, legs can be raised 




nearly to right angles with the body, no loss of joint sensation, 
no loss of sense of position. Pupils 2 mm., equal, irregular out¬ 
line, inactive to light and pain, active to accommodation. When 
looking straight forward, the pupils dilate upon his entering into 
conversation. He tells me he has the sensation of everything 
appearing very large. This statement he volunteered. Colour 
vision is good, he can read small print, and the fields are not 

Expression anxious and depressed, but when conversing, his 
face becomes very animated and emotional, and there is tremor 
in the lips. The tongue also is tremulous, the speech, however, 
is but very slightly affected. There is no history of fits before 
admission or since. He has had no feeling of constriction round 
the waist, and there is no difficulty with the water or the bowels. 
No scar or enlarged glands can be detected, but there are numerous 
small-pock-like scars on the forehead and a few on the legs. I 
could detect no cutaneous anaesthesia. His handwriting is good, 
and like his speech flowing and not tremulous, but it does show 
slight cutting up of syllables, (?) pathological. 

Mental condition .—When brought to the asylum he was sing¬ 
ing the Marseillaise with patriotic fervour. He is now full of 
grandiose delusions, some of which have a basis of truth, e.g ., he 
says that he is a great singer. He illustrated this by singing 
several songs in French with considerable expression, excellent 
articulation, and with a fine resonant voice. He then burst 
forth into the Marseillaise, singing it with extraordinary stirring 
patriotic fervour, suiting the action to the words. He was very 
pleased with his own performance, and spoke of kings, diamonds, 
and wealth. During his conversation, the muscles of expression 
associated with hilarity were especially brought into play, and the 
pupils dilated, but on ceasing, the same wearied lack of expres¬ 
sion occurred. 

August 20.—Patient in a side room, pale and emaciated, 
continually talking to imaginary persons, making lunges at the 
wall, or jerking his hands in the air as if throwing off some 
imaginary objects on his body. For the last few days he has 
employed himself rubbing his skin, especially of the knees and 
feet, with his shirt or bedclothes, muttering “ electricity.” He; 
has thus caused several sores on his body. These symptoms 
indicate auditory and visual hallucinations and lightning pains in 
the legs. 

The patient became very emaciated and died September, 1902. 
The brain showed characteristic signs of general paralysis, and , 



the spinal cord exhibited early tabic degeneration of the posterior 
columns in the lumbo-sacral region, and slight sclerosis of 
Goll’s column in the dorsal and cervical regions, after hardening in 
Muller’s fluid. 

Case 38.— Tabetic general paralysis , onset of tabetic and mental 
symptoms apparently simultaneously , arrest of tabetic con¬ 
dition , but slowly progressive dementia, symmetrical perforating 
ulcers of feet , knee-jerk absent on right side , present on left , 
speech for a long time only slightly affected , moderate exalta¬ 
tion and incoherence , knoivledge of time and place 'not markedly 
affected . 

W. D., aged 38, butler, married, with six children, admitted 
to Colney Hatch, November, 1897; history of six months illness, 
and certified as suffering from early tabetic general paralysis, his¬ 
tory of syphilis at the age of 16, pigmented scar of old gumma on 

Physical condition .—Tall powerful man, walks with rather a 
wide base, heels down first, but no incoordination or jerkiness in 
his movements, can stand with his eyes shut, knee-jerk absent on 
the right side, present on the left. He can touch the tip of his 
nose with the forefinger of the left hand, but not accurately with 
the forefinger of the right. 

Speech, no slurring of syllables, but slight hesitancy, can 
utter test words and sentences fairly well, without elision or slur¬ 
ring of syllables. There is no tremor of lips, and very slight of 

Mental condition .—Mild dementia and confusion, but no 
marked loss of knowledge of time or place. He has delusions, 
but there is a substratum of truth, e,g ., he says he knows all 
languages. Having been in the service of the French Ambassador 
as butler, he has probably heard many languages spoken, and 
doubtless, occasionally picked up a few words ; certainly he knows 
a few sentences of French, German, and Italian, but he fails to 
understand simple questions put in French or German, although 
he will make an attempt to reply in the language by which he has 
been addressed. A few months after he had been in the asylum 
he developed two symmetrical perforating ulcers of the feet. The 
ataxy did not increase, but the dementia slowly progressed. He 
had no fits. 

In October, 1899, he told me his age was 27, that he had a 
daughter who was married. There is a little more speech 



affection, and the attendant says he is very restless at night, get¬ 
ting up continually to make his bed and brush out the flies which 
he imagines are walking over him (?) formication. He appears to 
feel pricking and touch in all parts of his body, but it is difficult 
to be certain on account of his mental condition. 

November 14, 1900.—The left foot and leg are much swollen 
owing to an infective cellulitis, the knee-jerk on this side is still 
obtainable, but is absent on the right. The speech is more 
hesitant and slurred, knowledge of time and place more defective, 
and he now has grandiose delusions of wealth. He states that 
he has lots of money in the bank, and he will present each of us 
with a gold watch. 

June 1, 1901.—Dementia more marked, has a delusion that 
he is the Prince of Wales, expression exalted. Nutrition fairly 
good, appetite ravenous, knee-jerk cannot now be obtained on 
either side. Pupils each measure 3Jmm., irregular in outline, 
inactive to light, but react to accommodation. For a long time 
past he has persisted in getting up in the night to make his 
bed, he continually brushes the sheets. When the attendant 
asked why he did this, he said there were flies in his bed 
walking over him; very possibly this is a delusion based upon 
formication, owing to the cord affection. 

Case 39.— Advanced tabes of at least four years' standing . Delu¬ 
sions of persecution and auditory hallucinations then developed 
with mental excitement . Slight organic changes in the brain , 
especially of the f rontal lobe 9 most advanced spinal sclerosis in 
posterior column . 

L. W. K. Admitted February 1, 1900. Stockbroker’s 
accountant, aged 50. Single. 

Previous history (from brother on July 13, 1900).—Maternal 
grandfather drank heavily, and a distant relative has been in Earls- 
wood for more than thirty years. He had syphilis between 
twenty-five and thirty years ago. Abstemious for many years, 
but previously drank. He has had a considerable amount of 
mental worry. During the past two years at least, and probably 
for three or even four, he had walked very badly, raising his feet 
high from the ground ; the pupils of his eyes were like pinpoints. 
His present mental condition began quite suddenly just after 
Christmas, 1899. Shortly before Christmas he seemed very jovial 
and behaved in an artificial manner, and a week after Christmas 
he began to ramble in his conversation. He said that people 



were posting notices on walls about him. He told his brother 
not to go to his office, as there was a conspiracy against him. 
He wandered from home for the whole of one day, but returned 
of his own accord. He slept badly during the week referred to, 
he was then admitted into Hammersmith Infirmary, and a week 
later was transferred to Claybury. 

Facts stated in certificates .—Patient is excited, hears voices, 
says there is a conspiracy against him, that his brother has stolen 
his money, and that he knows himself that he is suffering from 
hallucinations. He jumps up in bed at night and calls out. 
Brought to the asylum in a straight jacket. 

Present state — Physical .—Height 5 feet 7 inches, weight 9 stone 
4 lbs. Two broken ribs on left side. Tongue coated, appetite 
good. Bowels irregular, urine and viscera normal, pupils irre¬ 
gular, contracted, and do not react. Unable to stand with eyes 
closed, gait tabetic, knee-jerks absent. Mental. —Dazed, lost, 
confused, and depressed, very restless, and constantly wandering 
about, short-tempered, impulsive, violent, and given to striking 
out at the attendant. He hears imaginary voices accusing him 
“ of stealing and owing money,” heard “ his brother groaning in 
the next room,” sleeps badly, but takes his food well, and is clean 
in his habits. 

Is suffering with mania and from tabes, is emotional, and his 
statements are contradictory and incoherent. He believes there 
has been, and there is a conspiracy against him for stealing a 
young lady's jewels, and assures me that it is false. His memory 
is impaired. He believes that some one is pointed out to him as 
his brother who is not, and he has aural hallucinations. He is 
full of nonsense about a certain young lady, and the wrong he 
has done his brother. He feels that his food has been tampered 
with for years, because he has seduced his mother's servant and 
given her syphilis, and says that her husband has been following 
him to take his life. He is in poor health and fair nutrition. He 
cannot stand with his feet together blindfolded. His gait is 
tabetic, his pupils are contracted, pinpoint, and inactive. He 
admits syphilis twenty-five years ago, he complains of shooting, 
neuralgic pains in his legs for some years, although nothing, he 
states, is to be seen. 

February 21, 1900.—Impulsive, quarrelsome, and violent, but 
does not now appear to be troubled with auditory hallucinations. 

April 30, 1900.—He is considered to be a general paralytic. 
Signs of progressive dementia. 

August 1, 1900.—He is now constantly wet, and very ataxic. 



October 23, 1900.—Stamps with his heels in walking, and 
throws his legs about somewhat, tongue very tremulous, speech 
rapid and slurred and without “ r’s.” He is failing very rapidly, 
and is very wet and dirty in his habits. The knee-jerks are 
absent, there is hypotonus to the extent of 20° beyond the ver¬ 
tical. When relaxed, the right pupil is If mm., and the left is 
If mm., the pupils rapidly accommodate, the right to 1 mm., and 
the left to 1 mm. Both pupils are irregular and inactive to 

October 30, 1900.—Kapidly became feebler, and died this 
morning at 9.50 a.m. 

Abstract of notes of post mortem .—Poorly nourished, bedsores 
on both buttocks and over sacrum, doubtful scar on glans penis. 
Head .—Skull cap dense, dura mater natural at the vertex, thin 
brown film above the tentorium and in the anterior and middle 
fossae, and most marked on the left side. Slight excess of sub¬ 
dural fluid, pia-arachnoid somewhat thickened, and strips rather 
more readily than natural. No adhesions in the mid line of the 
pre-frontal region, but there is considerable granularity of the pia 
in this situation. The pia here is also adherent to the subjacent 
cortex, which is congested. The basal vessels are natural. There 
is no definite change in the optic nerves ; the left olfactory tract 
appears to be smaller than the right, and both seem to be smaller 
than natural. Brain weighs 1,395 grams, natural, except for some 
fronto-parietal wasting. Each hemisphere weighs 600 grams, 
cerebellum and pons weigh 175 grams; the brain having been 
weighed without draining, this only leaves 20 grams of fluid. 
The hemispheres are normally convoluted. The cortex is dark 
and congested ; the rest of the brain is not congested, but the 
whole is somewhat wet, without the condition being that of 
definite oedema. The lateral ventricles are slightly dilated, and 
contain a few doubtful granules. The fourth ventricle throughout 
its extent appears to be covered with small granulations. After 
the hemispheres had been in formol for two days, and the 
ependyma had become hardened, all the ventricles were obviously 
granular. Cartilages natural, ribs brittle. On each side of the 
thorax there was evidence of*old-standing fracture of five or six of 
the lower ribs in front of the mid axillary line. No pleural 
adhesions. Both lungs broncho-pneumonic and oedematous. 
Throughout the aorta was a large amount of atheroma (first and 
second stages) ; there were no calcareous plates, but numerous 
pearly-white patches of fibrosis. Ureters inflamed throughout 
their course, acute cystitis, testicles natural. The brain, after 



having been hardened in Muller’s fluid, showed some thickening 
of the pia arachnoid over the motor area, particularly the upper 
part, and Broca. The above-named convolutions were shrunken. 

Microscopical examination of the brain .—Sections stained by 
Nissl method showed acute changes in the small, medium, and 
large pyramids, and overgrowth of glia cells. There was some 
cell proliferation of the perivascular lymphatics in Broca’s 
convolution. The left ascending frontal and parietal showed 
glia cell proliferation, especially in the deeper layers of the 
cortex, acute degenerative changes in the nerve-cells, and dis¬ 
placement of Meynert’s columns. In the posterior part of the first 
left temporal there was very little change observed; the same 
applies to the calcarine. Orbital mesial surface.—The vessels 
showed abundance of plasma cells in the lymphatic sheaths. 
The pyramidal cells had lost their normal shape, and many 
of them were atrophied, but there was no marked glia cell 
proliferation in this region. 

Marchi method .—A slight amount of recent degeneration was 
observed in the white matter. In the ascending frontal and parietal 
there was considerable recent degeneration of radiating fibres, more 
obvious than usually met with in general paralysis cases ; fine 
black dots could be traced into the second layer, but, probably, 
these fibres do not come from the pyramids of the third layer. 
Nothing noteworthy is to be seen in the first temporal or calca¬ 
rine ; only a few degenerated fibres can be seen, but they are 
practically inconsiderable in number, compared with those of 
the fronto-parietal region. 

Marchi-Pal. —Broca’s convolution.—The tangential and super- 
radial fibres are absent, and the interradial diminished in number. 
Base of first frontal, ascending frontal, ascending parietal.—In 
the first-named convolution the tangential fibres are absent, in 
the other two they are greatly diminished, and in places absent 
altogether. The super and interradial fibres are less affected 
than the tangential, but they are diminished in number ; there is 
no thickening of membranes and but little congestion of vessels. 
First temporal convolution—there is a marked diminution of 
tangential fibres, less of superradial and interradial. t There is no 
apparent thickening of membranes or vascular change noticeable. 
The same remarks apply to the occipital lobe in the region of the 
calcarine fissure, except that the vessels are passively congested 
(due to position). In the orbital lobe the tangential and super- 
radial fibres are entirely gone, and the interradial greatly 
diminished in number, the cells stained with osmic acid as if they 



were undergoing fatty and pigmentary degeneration. The spinal 
lesions are shown in the accompanying diagram which explains 
itself. It may, however, be remarked that each segment of the 
cord was examined and drawn by means of an Edinger projection 
apparatus, and it will be observed that there is no appreciable 
flattening of the posterior surface of the cord, although there is 
very obvious shrinkage in the transverse diameter of the posterior 
column. This also is shown strikingly in the photomicrograph. 
From the second to the eighth dorsal there is almost complete 
absence of fibres in the posterior roots at their attachment to the 

Fig. 27. 

Section of spinal cord at level of eighth dorsal segment. There is no 
flattening of the posterior column; it is even more convex than normal. 
There is, however, very marked shrinking and distortion of the gray matter 
and of the posterior column, so that the columns of Clarke are almost in 
apposition. The fibre plexus around the cells is completely atrophied, but 
encircling the columns are two sets of fibres, one external, proceeding from 
the gray matter of the posterior horn, the other internal, continuous with the 
fibres of the postero external zone. 

Magnification 16. 

cord, and in the same region a very complete degenerative atrophy 
of the exogenous fibres in the same regions of the cord. The de¬ 
generation below this eighth segment is not so marked but still 
very extensive. The endogenous tracts are atrophied but to a 
much less degree. Black indicates complete absence of fibres, dots 
partial absence. It will be observed that there is scattered crossed 
pyramidal degeneration which, however, cannot be traced above 



the mid-dorsal region. The posterior spinal ganglia showed 
only some pigmentary atrophy of the cells. The fibres distal to 
the ganglia were normal, whereas the central proximal fibres 
were completely or nearly completely devoid of myelin or had 
entirely disappeared. It was noticed that, whereas the myelin 
could be seen on some of the attenuated fibres, as they pro¬ 
ceed centrally from the ganglion, after a short distance it 
seemed to disappear. The atrophy of the fine plexus about 
the cells o t Clarke’s column was very extensive, indicating 
marked affection of the cerebellar path. Lissauer’s zone was 
also pretty extensively atrophied in the lumbo-sacral region; 
it was, however, variable on the two sides and at different levels, 
corresponding pretty closely with the degree of atrophy of fibres 
in attached roots. 

Nerves .—Right posterior tibial. Longitudinal and transverse 
sections show some degenerated fibres, but the degeneration 
appears to be not the Wallerian degeneration, but a swelling and 
opacity of the myelin in many of the fibres by which it stains 
imperfectly. Some of the fibres show merely empty primitive 
sheaths, and in longitudinal section these fibres are seen at 
intervals to exhibit coagulated balls of myelin or smaller myelin 
droplets. The anterior tibial nerve shows this change even 
more distinctly. 

Transverse sections of the sciatic nerve show paucity of fibres 
in many of the bundles, but whether there is a real atrophy or not 
it is difficult to decide. 

Skin of great toe—very few small bundles of nerve-fibres are 
seen, certainly less than normal. Examined with a high power 
one sees not more than one-third of the fibres are stained blue. 

Degeneration of the peripheral nerves, especially of the 
remote parts does exist, but it is inconsiderable as compared 
with the posterior roots. 

Optic nerves—transverse and longitudinal sections show by 
Marchi method many recent degenerated fibres scattered over the 
whole field, but more marked at the periphery, where also could 
be seen many bundles showing advanced atrophic degeneration. 

Case 40.— Ataxy with slight mental symptoms , altered respiration 
from failure of synergic action of muscles of abdomen , complete 
destruction of all the fibres of the posterior roots in the lower 
dorsal region of the cord . 

P. S., aged 61, married, chairmaker; has had seventeen 
children, fourteen living. He had syphilis at the age of 25. He 



was treated for it medicinally for a long time. His symptoms 
began with lightning pains, some years ago, exact time not 
known. He had been a considerable time in the infirmary, and 
was admitted to Colney Hatch, May 28, 1896, for mania. 

Present condition .—No discoverable mental symptoms, except 
feeble-mindedness, he is markedly ataxic, muscles greatly wasted, 
has girdle sensation, lightning pains, knee-jerks absent, plantar 
reflexes absent, abdominal reflexes greatly diminished on left, 
absent on right side. Argyll-Robertson pupils. There is 
loss of muscular power in the legs, and marked hypo- 
tonus, but his arms still possess considerable strength. There 

Fig. 29. 

is marked incoordination of the lower limbs. With his fingers 
he can readily touch the tip of his nose, when his eyes are 
shut. The belly is retracted, and there is complete atrophy of the 
left, and partial atrophy of the right quadratus lumborum and 
oblique muscles. Upon taking a deep respiration the lower ribs 
are drawn inwards, and a groove is formed {vide photo.). There 


is also great atrophy and weakness of the muscles of the lower 
extremities, they react to faradism, but require a stronger current 
than usual. There is no absolute loss of sensation anywhere in 
the legs, but it is much delayed and blunted, and there is numb¬ 
ness of the soles of the feet. The trunk was not tested; there 
is also complete absence of sexual power, and loss of control of 
bladder and rectum. There are symptoms pointing to rectal 
crises, but no gastric, larnygeal or other crises. 

July 1, 1896.—Condition of patient much the same, but there 
has been gradual loss of muscular power, and he is now bed¬ 
ridden. Left abdominal reflex is now quite absent. (F. W. M.) 

October 14, 1896.—Patient died to-day of exhaustion. 

Autopsy .—Fifteen hours after death. Body extremely wasted, 
and there is a large bed sore over the sacrum. The viscera 
presented no signs of disease except the bladder, the mucous 
membrane of which was thickened and inflamed. Naked eye 
sclerosis was visible in the posterior columns of the spinal 

Microscopical examination (by Dr. Hamilton Wright) — 
Brain .—Some pia-arachnoid thickening in frontal and central 
regions, with chronic atrophy of superficial fibres belonging to 
tangential and supraradial systems. Spinal cord.—Cervical 
enlargement .—The postero-median columns are denuded of 
fibres, and markedly sclerosed, except at their extreme apices, 
in the position of the endogenous cornu commisural zone. The 
inner halves and almost the whole of the median parts of the 
postero-external columns, show marked sclerosis, with a very few 
fibres only left. A few fibres have disappeared from the root 
zones, and they are slightly sclerosed. Lissauer’s tract on both 
sides is partially atrophied. There is a partial atrophy of the 
roots of this region, external to the cord. Many of the fibres still 
in situ are undergoing degeneration, and there is some fibrous 
tissue substitution. The right lateral column presents a marked 
degeneration, confined in the main to the anterior extremity of 
the direct cerebellar tract. The whole of this tract, however, is 
the seat of a diffuse fibre atrophy and sclerosis. On both sides 
there is a slight degeneration of fibres and sclerosis of the crossed 
pyramidal tracts. The Weigert-Pal method, which was employed 
for this investigation, revealed no degeneration in any part of the 
gray matter. Many anterior cornual cells are shrunken and 
much pigmented. There is a slight rarefaction in the posterior 
horns, probably the result of the few posterior root-fibres which 
course through them. 




Thoracic region .—At this level there is a marked atrophy 
of fibres in the postero-median columns. A few only are left, 
and these are in a state of chronic atrophy. The postero¬ 
external columns, except in the most anterior parts, and along the 
median margin of gray matter, exhibit marked sclerosis. The 
fibres of Lissauer’s tract have wholly disappeared ; all these parts 
are the seat of a marked sclerosis. A few fibres are left in the 
position of the cornu-commissural zone. The comma tracts are 
almost totally atrophied. The extra-cordal portion of the pos¬ 
terior roots contain no sign of nerve-fibres, but only a scattered 
debris . On the right side of the cord the crossed pyramidal tracts 

Fig. 30. 

Section of spinal cord at level of lowest dorsal region. There is complete 
atrophy of Lissauer’s tract extending into the region of the direct cerebellar 
tract, each side of which is also atrophied. The entering root-fibres have com¬ 
pletely disappeared. The fibres in the posterior column are mainly 
continuous with the two bands of fibre which encircle Clarke’s column, and 
are in all probability endogenous. The fibre plexus around the cells of 
Clarke’s column is completely atrophied. The central canal is dilated. 

show an atrophy of quite one-third of their fibres, and are deeply 
sclerosed. There is only a slight atrophy and sclerosis in this 
tract on the opposite side. Both posterior horns are greatly 
wasted. In the right horn no proper tissue is to be observed 
dorsal to its neck. The opposite horn contains here and there a 
sign of proper tissue posterior to Clarke’s column. Clarke’s 
columns are denuded of fibres of all kinds. The right column of 
Clarke contains no evidence of nerve-cells, except in the lower 
segments, and even here they are greatly shrunken and deeply 
pigmented. A few only are to be observed in the opposite 



column, all greatly shrunken and pigmented. The posterior gray 
commissure contains only a few vestiges of fibres. The gray 
matter of the anterior horns is shrunken and rarefied, its cells are 
deeply pigmented and exceedingly few in number. The anterior 
roots on the left side are almost totally atrophied. On the oppo¬ 
site side a few fibres are still to be observed. Lumbosacral 
region .—The only fibres left in the posterior columns of this 
division of the cord are in the position of the cornu-com¬ 
missural zone, along the median margin of the left posteridr 
horn and in the left root zone. Even here they are few, greatly 
attenuated, or irregularly swollen. All other parts are intensely 
sclerosed. There is no sign of the median triangle of Flechsig, 
or the sacral fibres of Gombault and Phillippe. This is an 
important point in view of the sphincter paralysis. The posterior 
roots on the right side are totally atrophied. A few extremely 
wasted are still present on the left side. In the lateral columns 
of this level the atrophy of fibres, and the consequent sclerosis is 
apparently not so great as in the thoracic region. It appears to 
be equal on the two sides. The posterior horns contain only a few 
fragments of fibres in the substantia gelatinosa. The cells appear 
to have totally atrophied. The necks of the posterior horns are 
greatly rarefied and sclerosed. Only a few remains of fibres are 
present in the posterior gray commissure, and none of these appear 
to bend backwards along the posterior median septum. The 
anterior cornual cells are shrunken and are deeply pigmented ; it 
k difficult to decide whether any have totally wasted and 
disappeared, but it is not unlikely in view of the state of the 
anterior roots. On both sides the root-fibres have in great part 
disappeared, and the majority of fibres that remain are attenuated. 
'The piamater is thickened, and the superficial layer of neuroglia 
beneath it appears to be augmented throughout the cord, es¬ 
pecially where the sclerosis is marked. There is a great congestion 
of the pial, and deeper vessels; thickening of their coats has 
occurred in the pia, and in those parts of the cord where atrophy 
•of fibres has been followed by sclerosis. Posterior spinal 
ganglia in the cervical region were not examined. In the 
thoracic and lumbo-sacral levels there is considerable degeneration 
of the cells. The most noticeable feature is a general pig¬ 
mentation ; in many instances no vestige of the cell is to be seen, 
and the capsule is full of dark brown pigment. Many cells have 
stained purplish blue by the Weigert-Pal method, indicating fatty 
degeneration. A few cells are reduced to a granular debris, in 
the centre of which is a turgid granular nucleolus, the nucleus 



having entirely disappeared. The capsules are thickened, and the 
general interstitial overgrowth is marked. The vessels are 
congested, and their walls slightly thickened. 

Case 41.— Tabes , probably of some standing , homicidal and suicidal 
mania , grandiose delusions. Ataxia , mental and physical 

improvement , obvious ataxy disappears , attack of suicidal 
mania , left-sided convulsions , tremor of face muscles , but little 
speech affection . Death from mtercurrent disease two years 
after admission. Naked eye and microscopical examination of 
brain and spinal cord exhibits first stage of ataxic lesion of 
cord and roots , heterotopia of central canal in lumbo-sacral 
region. Changes in cortex cerebri of gemral paralysis. 

H. J. B., telegraphist, aged 41, admitted to asylum, Cane Hill, 
December 28,1897. Died December 14,1899. Medical certificate 
states that he had threatened to shoot his wife and then himself. 
Before admission to the Infirmary he had been excited and 
emotional. He had suffered with unbearable pains, he had been 
the subject of grandiose delusions, pawned nearly everything for 
drink, stolen billiard balls, brushes and other articles. 

History. —First attack. Duration of mental symptoms two 
months; first symptom noticed, sleeplessness and loss of flesh—has 
locomotor ataxy which began nine months ago; supposed cause, 
alcohol; married ten years, two children. No phthisis, insanity, 
or alcohol in family history. States himself that he had a soft 
sore for which he was treated with medicine for two months. 

Physical condition. —Nutrition good. Tongue tremulous. 
Pupils unequal, Argyll-Robertson. Deep reflexes absent. Plantar 
present, marked. Gait, walks with a wide base. Romberg 
sign. Complains of pains, no visceral disturbances. No evidence 
of organic disease of abdominal or thoracic organs. 

Mental condition. —Talkative, rambling, irrational. He has 
exalted notions of his powers as an athlete, musican, and 
elocutionist, but I found that these are not strictly delusions, but 
exaggerations of undoubted faculties possessed by him. He has, 
however, true grandiose delusions, for “ he possesses a gold 
mine.’' Speech somewhat hesitant and tremulous, especially of 
lip explosives. 

After some weeks he improved mentally and physically and 
nine months after admission he was able to work in the fields 
five hours a day. 

June 19, 1899.—The notes state that he has been having 



convulsive seizures, and six weeks ago he had an attack of suicidal 
mania, attempting to mutilate himself and gouge out his eyes. 
There is now more dementia indicated by the blank facial 
expression and his conversation. He does not respond regularly 
to the calls of nature. Tremor of facial muscles more marked. 
Beyond walking with a wide base no sign of ataxy. He is dan¬ 
gerous to himself and others. 

December 5, 1899.—Patient helpless, bedridden, and de¬ 
mented ; death occurred a week later from broncho-pneumonia 
and cystitis. 

Autopsy (summary of notes).—Old scar on glans penis, no 
bed sores. Skull cap thick and dense. Dura mater adherent to 
pia-arachnoid over central convolution of left side. Pia-arachnoid 
of pre-frontal and central convolutions, thickened, opaque and 
milky. Some wasting of convolutions and cortex somewhat dim¬ 
inished. Fourth ventricle dilated, granular ependyma. Brain— 
right hemisphere 17 J ozs., left 17£ ozs. Cerebellum and pons— 
5 ozs. 

Cause of death .—Broncho-pneumonia, cystitis and pyo¬ 

Microscopical examination (summary).—Atrophy or absence 
of tangential and superradial fibres in various situations of 
atrophied convolutions, marked vascular congestion, with num¬ 
bers of plasma cells in perivascular lymphatics. Atrophy and 
degeneration of small and medium sized pyramids. Glia cell 
proliferation. Spinal cord .—Some leptomeningitis not more 
marked posteriorly than anteriorly, the same applies to vessels 
which are congested and their walls thickened. In cervical 
region the degeneration is limited to Goll’s column. By Marchi 
method there are scattered fibres degenerated in all the white 
matter. In upper dorsal and mid dorsal regions there is exten¬ 
sive atrophy of root-fibres and their intraspinal projections. 
In lower dorsal region there is also some diminution of fibres 
in the comma tract. Lissauer’s zone is most affected about 
the fourth and fifth dorsal, where the roots are most denuded 
of fibres. About the eighth dorsal, but not above this, there 
is obvious sclerosis of the crossed pyramidal tracts, which 
becomes more obvious as we proceed downwards. In the lowest 
dorsal and lumbo-sacral regions the roots are not so markedly 
affected and the degeneration in the posterior column takes the 
characteristic winged appearance, the apex of the wing on either 
side corresponding to the root zone. There is not a marked 
atrophy of the fine plexus around the cells of Clarke’s column. 



A more than usual number of coarse fibres persist in the 
sclerosed posterior roots. The endogenous fibres in this region 
are but little affected. At the level of the fifth lumbar segment 
and extending into the sacral segments is a dilation of the central 
canal which extends back as far as the posterior surface. This is 
not an artefact for it is lined with the characteristic epithelium, 
and represents a congenital failure to close up the canal in this 
region by the ingrowth of fibres. At the posterior surface and 
corresponding to the mesial line is an agglomeration of vessels, 
dense fibrous tissue and a few bundles of embryonic muscle fibres . 
In the fibrous tissue also there are scattered groups of ganglion 
cells, and small nerve-fibres. The cord in this region, and, indeed, 
throughout the lower dorsal and lumbar region is very small. 
One structure, however, is not diminished more than another. 
It appears to be a failure in development. In a section of the 
last lumbar spinal ganglion, in what corresponds to the white 
ramus are a group of cells which stain slate blue with the Weigert 
method, and from these issue a number of coarse medullated 
fibres. Whether this is an abnormal condition I am unable to 

Conclusions are (1) that this patient had thoracic cutaneous 
anaesthesia, had it been looked for; (2) That the ataxy was not a 
permanent feature of the clinical symptoms, because there was 
neither marked atrophy of the fine plexus around Clarke's 
column, nor was there much atrophy of the lumbo-sacral region, 
except of the fibres concerned with reflex spinal tonus; moreover 
the endogenous fibres were not affected in the lumbo sacral 
region. Therefore, the ataxy that existed was due more especially 
to a condition which might under circumstances vary, viz., the 
reflex spinal^onus and its inhibition by cerebral influence. 

The general atrophy of the cord indicates a general nutritional 
defect; this is frequently met with in these cases of tabo-paralysis, 
but in this case it might have been congenital. 

Case 42.— Tabetic general paralysis , with characteristic pathological 
changes affecting the brain , spinal cord , posterior roots, and 
optic nerves . Marked degeneration of fronto-occipital and 

frontotemporal association tracts, causing dilatation of lateral 
ventricles . 

J. H., aged 37, occupation a tailor, admitted to Clay bury, 
June, 1899. 



Abstract of notes .—Married eleven years, three children, two 
alive, one dead. Wife states that he had fits, and had complained 
of pains in his legs for two months prior to admission. There 
was a history of insanity on the father’s side. 

Mental state on admission. —He is noted as being strange in his 
manner, wandering constantly from one subject to another, so 
that it was difficult to obtain from him a coherent account. He 
states that he hears voices talking to him at night. He has no 
idea of time or place, and he believes that his wife and family live 
here. He is under the delusion that he has murdered some of his 
children by strangulation, and he wants an operation performed 
on his legs, presumably on account of the pains. 

Physical state. —There is marked shortening of the right leg, 
the muscles of which were very wasted, and there is evidence of 
old hip disease, (?) Charcot’s joint. There are patches of alopoecia 
on the head, and he states that he has had both gonorrhoea and 
syphilis. The knee-jerks are absent, and the left leg is retro- 
flexed, jerking and ataxic in movement. The pupils are unequal, 
the left being dilated and sluggish in reaction to light and 
accommodation ; the right pupil reacts fairly readily. There is 
well-marked primary optic atrophy on both sides, more obvious in 
the left eye. Diagnosis at first was mania; towards the end of 
the year he commenced having seizures affecting especially the 
right side, the diagnosis of general paralysis was then made. At 
the end of January, 1901, he died of pneumonia and cardiac 

Post-mortem examination. —Body is well nourished, no external 
marks of syphilis, right leg 3 inches shorter than the left. Skull 
dense, excess of fluid in subdural and subarachnoid spaces. The 
pia-arachnoid was thickened and opaque in the frontal and fronto¬ 
parietal regions, convolutions were atrophied, though not markedly 
so ; on stripping erosions were seen. The lateral ventricles were 
granular and dilated. The fourth ventricle was also granular. 
There was well-marked atrophy of both optic nerves. 

Cause of death: (a) Primary. —Broncho-pneumonia and 

gangrene of lung. (&) Secondary. —Tabetic general paralysis. 

Examination of spinal cord by Marchi and Marchi-Pal methods 
showed by the former a number of recent degenerated fibres 
in the crossed pyramidal and direct tracts, also scattered generally 
in the posterior columns. The degenerated fibres were seen at all 
levels of the cord, and were probably therefore mostly belonging 
to long systems. By the Marchi-Pal method denudation of fibres 
and subsequent sclerosis with a moderate proliferation of glia 



tissue was found in the posterior columns of the spinal cord. In 
the cervical region this was almost exclusively limited to the leg 
fibres forming the column of Goll. In the lumbo-sacral region, 
where the denudation of fibres- and subsequent neuroglia over¬ 
growth was most marked, the atrophy of fibres was limited to 
exogenous systems. The only part of the posterior columns 
which did not show denudation of fibres was the cornu-com¬ 
missural zone and the median oval area. The short length fibres 
of Lissauer’s tract, the medium length cerebellar fibres, and the 
long fibres which together form Goll’s column, are in great part 
destroyed or atrophied. The fibres of the posterior roots in many 
of the sections show considerable denudation of fibres. In the 
upper lumbar and lower dorsal region there is still a great 
diminution of exogenous fibres entering into the formation of the 
posterior columns, and there is a corresponding overgrowth of 
glia tissue. The atrophy of the fibre plexus around the cells 
of Clarke’s column is only moderate. Cauda equina .—To 
the naked eye the sections show an obvious difference in 
the anterior and posterior parts. In the former the roots 
are of good size, and are stained blue, whereas in the latter 
the roots are atrophied and unstained. Examined microscopi¬ 
cally, the posterior bundles are considerably shrunken, and 
exhibit very few fibres. Some are apparently almost destitute 
of fibres, consisting only, or for the most part, of connective 
tissue. The anterior bundles (motor) are normal in appearance. 
In both anterior normal and posterior sclerosed roots there 
are many congested vessels. The walls of these vessels, how¬ 
ever, present no marked abnormality. 

Microscopic examination of brain .—Marked degeneration of 
fronto-occipital and fronto-temporal association fibres, atrophy of 
superficial cell layers of cortex in pre-frontal and fronto-central 
regions, slight glia cell proliferation, only small amount of 
vascular change. Atrophy of tangential and supraradial fibres in 
same situations. 

Case 43.— Tabes of four years standing , then a congestive seizure , 
followed by transitory aphasia and slowly progressive de¬ 
mentia . 

R. B., aged 50, admitted to Colney Hatch, September 12, 
1900. Ticket of leave man, sent from Pentonville, single, occu¬ 
pation tailor, working as a sewing machinist, previously in the 



Marines. Admits having had a sore on the penis, which gave him 
no pain, and he was not treated. Lymphatic glands generally 
enlarged, papery scars over chest and abdomen. 

History of illness .—Four years ago had a cord-like feeling 
round the waist, he has drunk heavily at times, but there is no 
marked history of alcoholism. 

Family history not obtainable from friends, as he has no 
visitors. He himself is unable to give any satisfactory data. He 
was transferred from Pentonville with a certificate, indicating 
that he had had a congestive seizure, followed by transitory 
aphasia, with dementia, and wet and dirty habits. 

Mental condition .—He has no actual delusions, he is a little 
incoherent in his answers, but can give a fairly intelligible account 
of his past life, although his memory as to place and time is 
-defective, for he does not know the year, nor the month, but he 
was able to tell me that he was in the Marines, and that he had 
been in Pentonville prison, where he was sent for having stolen a 
piece of meat. He can hardly do simple multiplication sums, 
and if able to give a correct answer, he is quite lost when the 
figures are reversed. 

Physical condition .—There is a loss of expression of the face, 
especially of the right side, the right grasp is a little feebler than 
the left. The speech is very slightly hesitant, no tremor of 
tongue or lips. He has a very ataxic walk, and he cannot stand 
with his eyes shut. He has pain in his legs, which he thought 
were rheumatic; he has suffered with them for twelve months, 
and thought that they were due to the machine work. Right 
pupil irregular, rather smaller than the left (3mm.), inactive to 
light, they react to accommodation. He has some loss of sense of 
position in the hands and feet, he can correctly locate light tactile 
sensations, and he recognises the prick of a pin over the whole 
body. The leg can be raised to a right angle with the body, indi¬ 
cating a fair amount of hypotonus. The knee-jerks are absent on 
both sides. Examination of the fundus reveals nothing abnormal 
on either side. 

June, 1901.—There is very little change in the condition of 
this patient. He is somewhat thinner, but his mental condi¬ 
tion has not altered for better or worse. He walks more 
unsteadily and there is a tendency to fall to the right. The 
tongue is more tremulous and protrudes towards the right 
slightly. The pupils are unequal, the right 3J mm. irregular, 
the left 3 mm., also irregular, inactive to light, react sluggishly 
to accommodation. 



Case 44.— Tabes eleven years after infection. Ataxy , sensory dis¬ 
turbance , bladder disturbances , history of monetary troubles , 
development of mental symptoms , disappearance of spinal 
symptoms in great measure. Knee-jerks absent on admission 
to asylum. Mental and physical improvement. Relapse t 

development of left-sided seizures terminating in hemiparesis 
without any ccmtraction. Reappearance of knee-jerk on left 
side . Attack of dysentery , recovery. Attacks of vomiting 
(probably crises). Further left-sided seizures spreading to 
right side. Death two years after onset of mental symptoms. 
Right hemisphere 17J ozs. Left 19f. ozs. Naked eye gray 
degeneration of posterior columns of spinal cord , also of 
pyramidal track on left side in dorsal and lumbar regions. 

W. H., college porter, Guy's Hospital, aged 38. Married, 
two children, and two miscarriages ; contracted syphilis in 1888, 
for which he was well treated. No history of insanity in the 
family, not intemperate. In May, 1899, complained of pains in 
the legs and unsteadiness of gait. He was admitted into Guy’s 
Hospital under Dr. Pitt, to whom I am indebted for the following 
notes. Pains in the lower extremities, in the bones and muscles 
rather than in the joints. He complained of unsteadiness in walking, 
and he noticed diminution of sensibility across the buttocks and 
scrotum, and along the inner sides of the thighs. Thinks when 
he is sitting down that he is on a pole 3ins. in diameter. Marked 
ataxic gait, even with eyes open. Cannot stand with feet together 
and eyes shut. Knee-jerks absent. Plantar reflexes absent, 
abdominal present. Impaired sensation of soles of feet and inner 
sides of thighs. Pupils equal, small A.E. Speech normal. At 
times depressed, memory and intelligence good. Frequently he 
has difficulty in starting micturition, and is troubled with consti¬ 
pation. Frenkel's treatment applied with benefit; discharged 
in unchanged condition. 

His wife relates that he had saved £350 in eleven years, and 
he lent some of it to a friend who did not repay him, and this 
caused him great worry and anxiety, followed by sleeplessness 
and depression; his mind became affected, and he was admitted 
to Bethlehem in September, 1902, and to Cane Hill Asylum, 
December 31, 1900. His condition in February, 1901, was as 
follows :— 

Physical condition .—Facial expression denotes mental enfee- 
blement; there is some obliteration of the lines of expression, 
especially on the left side. The left eye is rather more open than 
the right. There is marked tremor of the tongue and lips, and 



staccato speech ; there is more tremor on the left than the right 
side. Eight pupil, 2 mm., left, 2§ mm.; right, accommodation to 
If, and left to 2. No reaction to light or pain. Gait slightly 
unsteady and incoordinate, rather a wide base, no stamping of 
feet, no Eomberg symptom, no definite area of affection of 
cutaneous sensibility to pain or touch anywhere (answers quite 
reliable); sometimes confuses a touch with a prick. No loss of 
sense of position of joints. A needle introduced deeply into the 
muscles of the legs in different regions, and the patient made to 
move the muscles, exhibited a loss of muscular sense. Plantar 
reflexes normal, all other superficial reflexes brisk. Knee-jerks, 
and triceps-jerks absent, hypotonusof hamstring muscles extreme 
(30 degrees beyond the vertical). No crises, no loss of control of 
sphincters, and no difficulty now with the bladder or bowels. 

Mental state .—Very emotional, readily laughs or cries. 
Marked bien etre , weak-minded and childish in conversation. 
Comprehension fairly good, likewise orientation. He can give a 
fairly good account of his past life, and he has no delusions, 
illusions, or hallucinations. 

For some time he improved both mentally and physically, 
then in April, 1902, he suffered with left-sided seizures and 
vomiting, which preceded an attack of acute dysentery; blood 
and slime in stools, pyrexia and distended tender abdomen. It 
was a month before the acute symptoms subsided, and two 
months before he was convalescent. During this period of 
convalescence he suffered with paroxysmal attacks of vomiting 
(crises?) on several occasions. In August he was much more 
demented, and was the subject of many epileptiform seizures, 
mainly affecting the left side, leaving him in a nearly hemiplegic 
condition; whether he was hemianaesthetic could not be de¬ 
termined, as he did not speak when questioned. 

The left knee-jerk was now obtainable , the right still absent. 

August 29.—He commenced a succession of epileptiform 
seizures affecting especially the left side (head and eyes turned to 
the left). Temperature subnormal. August 31.—The convulsions 
on left side ceased, the limbs were flaccid and helpless. Con¬ 
vulsive spasms of the right side now occurred, conjugate deviation 
of head and eyes to the right. Temperature 100*6°, quite uncon¬ 
scious ; death supervened on September 1. 

Autopsy (abstract).—No scar on penis or glands or signs of 
syphilis on the body. All the viscera were apparently healthy, 
with the following exceptions. Heart .—12 ozs., cavities dilated, 
stopped in diastole, muscular substance greasy and friable. No 



valvular disease. Lungs .—Healthy, excepting hypostatic pneu¬ 
monia of both bases. All the abdominal organs, like the thoracic, 
showed signs of congestion, the result of asphyxia from pro¬ 
longed seizures. Throughout the large intestine there was 
evidence of the attack of dysentery from which he had suffered. 
The mucous membrane was thin, and showed white lines and 
small patches indicating scar tissue, the solitary follicles were in 
many places prominent, but everywhere the condition denoted that 
a healing process had occurred, and there were no signs of recent 
affection of the internal coats of the bowel. Brain .—Excess of 
fluid, marked thickening of pia-arachnoid, especially over fronto- 
central convolutions, great wasting of right hemisphere. Weight, 
right, 17£ ozs. Left 19f ozs. Great dilatation of right ventricle, 
especially in posterior part, due to atrophy of brain substance, 
forming floor and outer wall ependyma granular. Convolution, 
pattern complex and good. Brain kept for investigation, fourth 
ventricle very granular. Spinal cord, obvious atrophy of posterior 
roots, and gray degeneration of posterior columns extending from 
the seventh and eighth cervical segment downwards. Degen¬ 
eration of left crossed pyramidal tract in lower dorsal and lumbar 
regions. Examination of blood contained in the femoral vein 
showed a great abundance of choline. 

Microscopical examination .—Brain exhibited marked cell and 
fibre atrophy, glia proliferation, and vascular changes, with 
plasma cells. 

Case 45.— Tabes of four years duration in a man aged 55. Arterio¬ 
sclerosis affecting the small cerebral arteries especially , 
marked atrophy of the right hemisphere , with multiple miliary 
softenings , left hemiancesthesia , and hemianopsy . 

C. C. Occupation, labourer and turner at the Arsenal; after¬ 
wards railway porter, and for thirty years a signalman. Aged 55. 
Married twenty-seven years, no children ; wife had two premature 
births. Drank somewhat when a porter, but not recently. His 
symptoms began three or four years ago ; he noticed difficulty in 
passing his water, which ran slowly, and he continually wanted 
to go, but the urine only dribbled away; also, he had difficulty 
with his bowels, and shooting rheumatic pains in the left leg. 
He gives a history of having had a sore on his penis four years 
before marriage. He was treated for three or four months at 
the Royal Free Hospital. He had secondary symptoms, sore 
throat, rash and hair falling out. He was admitted to Cane Hill 
Asylum with delusions of persecution. No insanity in the family. 



On October 4, 1900, he had an epileptiform seizure, which 
left him in an incoherent mental condition, and he could give no 
rational account of himself. 

Physical condition (October, 9, 1900).—He is in fair state of 
nutrition, and was able to give a good account of himself and his 
illness, which I subsequently found reliable. He is a well-built 
man with several papery scars over the back. He has an ataxic 
gait, the left foot and leg being most affected. The knee-jerks are 
absent on both sides even with reinforcement. There is marked 
hypotonus in both legs. Bomberg’s symptom is present; he has 
not suffered with any crises, and he complains of no visceral 
symptoms, except the difficulty of making water. The pupils are 
equal, perhaps the right a little larger than the left (2£mms.), in¬ 
active to light, react to accommodation. He has complained of 
imperfect vision in the left eye, and tested roughly, he is found to 
have left-sided hemianopy. He has had one left-sided epilepti¬ 
form seizure since he has been in. He says sometimes he will 
wake up and not know that he has a left leg and hand. He has 
been unable on account of the numbness to button his clothes 
with his left hand for four or five months. There is great inco¬ 
ordination in movements performed with the left hand. He 
cannot touch the tip of the nose, but he can do it with the right* 
hand. He says he cannot feel his moustache with his left hand, 
but he tells me of his own accord that he has no loss of power, 
and he certainly has a good grasp. His sensation was tested, and 
the accompanying charts indicate the condition found. It may 
be remarked, however, that although it took one hour and a half 
to make these charts, they can only be considered approximately 
true, for, as in all cases, response to stimulus varies ; but subse¬ 
quent notes made by Dr. Gilfillan show a marked difference in 
sensibility on the two sides of the body. Very possibly, the 
hemianaesthetic condition may vary in degree according to varia¬ 
ble conditions of the opposite hemisphere, but the post-mortem 
results absolutely accord with this condition. I saw the patient 
several times subsequently. I did not notice any speech affection 
or tremor of the lips and tongue, and I looked upon the disease 
as a case of tabes with mental symptoms. There was only a very 
mild degree of dementia, his knowledge of time and place and 
memory for ordinary events of his past life seemed fairly good. 
The attendant states that he is dull, confused and incoherent 
after he has had fits. 

December 15, 1900.—Had a slight seizure on November 30, 
followed by increased weakness of left leg. Had a seizure on 



December 13, and another to-day, affecting his left side. Is now 
confined to bed. 

February, 1901.—Knee-jerks absent. Plantar reflexes exag¬ 
gerated. Left leg paralysed, left arm weak (patient says it is 
senseless). Sensation right side good, whenever roughly touched on 
left leg, refers touch to inner side of thigh ; touched on left arm, 
refers touch to point of shoulder. Complains of pain and numb- 

Fig. 31. 


Diminished Cutaneous Sensibility 
to Pain and Touch 
Analgesia and Anaesthesia 

ness of left leg. Pain in left hip shooting down to knee and calf. 
Pain during passive movement of left leg. 

Girdle pains when up, never in bed. Shooting pains in left 
arm. Pupils equal. Left reacts to light sluggishly, both to 
accommodation. Tongue steady. Right side distinguishes hot 
and cold. Left side cold resembles pricking, and hot not 
recognised. (Dr. Gilfillan.) 



March 21, 1901.—Had a seizure to-day affecting the left side. 

April 17.—Has marked dulness over left lung, and impaired 
breath sounds. Temperature hectic in type. Feeble health. 

May 1,1901.—Small rales can be heard over both lower lobes, 
but the sounds are muffled in the left. Is rapidly becoming much 

May 7.—Gradually sank and died. 

o 0 O O 

0 ° ° O r> 

= Thermo-anasthesia 

-f 4- -f + 

9. Q.g -P 

+ + + + 

= Hyperaesthesia 

Cause of death as certified.—General paralysis of the insane. 
Tubercular broncho pneumonia. 

Abstract of post-mortem notes : Body well developed and 
well nourished, except thighs and legs, which are wasted and 
flabby; a large amount of subcutaneous fat present in all parts 
of the body. No marks of syphilis. Skull .—Nothing abnormal. 
Membranes .—Dura mater thickened and firmly adherent to skull 



along the vertex. Pia-arachnoid extremely opaque, much 
thickened, chiefly in frontal, central, and parietal regions. In 
places it is somewhat maroon coloured, probably the result of old, 
slight haemorrhages. The membrane strips readily without 
causing decortication. Pacchionian bodies are very large. 
Spaces .—Subdural contains excess of clear fluid ; sub-arachnoid, 
excess of fluid, which is slightly blood tinged. Brain .—The left 
hemisphere weighs 4 ozs. more than the right; the convolutions 
of the right hemisphere are of normal complexity, but markedly 
atrophied, especially in the frontal and central regions, the sulci 
here being wide and deep, containing considerable excess of fluid. 
The ventricles are slightly dilated, and studded with a few small 
granulations. The vessels, especially the branches of the carotids, 
are studded with numerous atheromatous plaques. The sinuses 
are healthy. The fourth ventricle is granular, but the cerebellum, 
pons and medulla, show no naked eye change. The general 
appearance of the right hemisphere of the brain is characteristic 
of general paralysis, the left to a much less degree, but vide 
description after hardening in Formol. Considerable excess of 
cerbro-spinal fluid. The left hemisphere weighed 600 grams, 
the right 490 grams, preserved for further examination. Extensive 
leptomeningitis affecting the posterior surface of the spinal cord, 
especially in the dorsal region. There is naked eye gray de¬ 
generation of the posterior columns in the lumbar and dorsal 
regions. The patient died from extensive tubercular broncho¬ 
pneumonia. The brain and spinal cord were hardened in Formol- 
Miiller solution, and then sliced up and examined. There was no 
naked eye foci of softening to account for the atrophy of the right 
hemisphere. Convolutions were much smaller on the right than 
the left side, and showed a considerable diminution of the gray 
matter of the cortex of the frontal, central, parietal, and temporal 
regions, where there was very marked thickening of the pia- 
arachnoid. The right lateral ventricle was markedly dilated, 
especially in the posterior part, and extended farther back than 
the left. 

Microscopical examination .—By Nissl, Marchi, and Weigert 
methods demonstrated the following facts. There was a random 
degenerative process due to vascular changes, which was the 
principal cause in the difference of weight in the hemispheres. 
The fact that no gross change could be seen, and yet there was 
so much atrophy, accords with the microscopic observation of 
numerous scattered miliary areas of softening in the white matter 
immediately subjacent to the gray cortex, affecting especially the 



radial fibres of the ascending parietal, and the optic radiations 
about the calcarine fissure. Sections through the ascending 
parietal and ascending frontal show a gross old degenerative 
change of the ascending parietal. This accords with the fact that 
there was a hemiamesthesia without much loss of power when I 
saw him. Later, no doubt, there was extensive destruction of the 
ascending frontal, or more likely some part of the path of the 
fibres on their way to form the pyramids of the medulla, for the 
left pyramid presented a naked eye atrophic sclerosis, likewise 
the right direct pyramidal tract. The spinal cord also showed 
atrophic sclerosis in the usual situation in the posterior column 
of a fairly advanced case of tabes. The miliary softenings in the 
brain show the following characteristics: dilated congested vessels 
with haemorrhages into the lymphatic sheaths, accompanied by 
endothelial cell proliferation lymphocytes and plasma cells ( vide 
Plate VIII., fig. 2). Many of the larger neoplastic cells contain 
pigment derived from the blood in various stages of disintegra¬ 
tion. In the neighbourhood of these vascular changes, which 
often have a dendritic form are seen ganglion cells undergoing 
acute degenerative changes. The miliary softenings are much 
more numerous in portions of the right hemisphere in various 
situations than in the left. They seldom affect the superficial 
layers of the cortex, hence in many regions where there is a 
very extensive destruction of the radiating fibres there is less 
destruction than one would expect of the tangential and super- 
radial fibres. The affection of the right hemisphere and the 
fact that the superficial fibres of the cortex were not much 
affected may account for the comparatively slight dementia he 
suffered with, as compared with the amount of brain destruction. 

Case 46.— Publican, formerly 'policeman, suffered five years with 
progressive tabes, development of mental symptoms, becoming 
lustful, suspicious, extravagant, and dangerous to himself and 
others. Speech affection developed, progressive dementia with 
intervals of improvement, epileptiform seizures, death. Ad¬ 
vanced tabic lesion of the cord, chronic and acute degenerative 
changes of the brain. Heterotopia spinalis. 

W. A. McSt., publican, aged 42. Married; no children. At 
17 joined the Guards, served eight years, became colour-sergeant. 
While in the army had gonorrhoea and sore. At 25 joined the 
police force, served thirteen years, invalided with locomotor 
ataxy. First symptom noticed was sudden loss of power in his 



legs, while serving notices as a jailor. After this suffered with 
pains in his legs and girdle sensations, no bladder trouble until 
recently; he has not suffered with headache nor any visoeral 
crises, does not complain of his food. 

Physical condition .—Ataxic gait, Romberg's symptom marked, 
triceps and knee-jerks lost, some loss of sense of position in 
hands. Right pupil 4 mm., left 5 mm., irregular, and neither 
react to light, but sluggishly to accommodation. He stands with 
a wide base and with the support of a stick. He has some diffi¬ 
culty in maintaining his position on the polished floor, and he 
finds a special difficulty in rising from a sitting posture. He has 
a typical ataxic walk, the body being bent forward, the neck 
stiff, but slightly inclined down, so that he can watch and control 
the movements of his legs. The advancing leg is extended at 
the knee instead of being flexed, jerked forwards and outwards at 
the hip, the heel being brought down with a stamping action. 

Expression .—He has a depressed and anxious look when not 
engaged in conversation, but he is easily moved to tears or 
laughter. When speaking there is a marked tremor in the lips 
noticed, and there is a tremor in the tongue on protrusion. His 
speech, like his handwriting, is hesitant, tremulous, and many of 
the syllables are Blurred. 

Shin sensibility .—Over the thorax, from the sixth to the tenth 
segments inclusive, there is a loss of sensibility to light tactile 
impressions. Above and below this region, he feels light tactile 
sensations, but there is often some confusion as to localisation, 
and on the peroneal surface of the legs and the soles and dorsal 
surfaces of the feet, light tactile sensibility is oonsiderably dim¬ 
inished, and often the stimulus is either not felt or incorrectly 
localised in these regions. Painful sensation is blunted con¬ 
siderably over similar regions to those in which tactile sensibility 
was impaired or lost. Very often there was a considerable delay 
(two or three seconds) before he responded to the stimulus. In 
the regions above and below the areas of analgesia pricking 
seemed to cause unusual burning pain, so that there was hyper- 
sesthesia over the inner side of the leg and thighs and lower part 
of the abdomen. I could detect no thermal-anaesthesia over any 
part of the body {vide charts of sensory disturbances). 

Reflexes .-—Triceps and knee-jerks absent; superficial reflexes— 
plantar present, but not active, cremasteric present, fairly active. 
He has had no difficulty with his bowels or bladder, he has no 
loss of control. There is some degree of hypotonus, but not in 
proportion to the ataxy. The muscles are firm and strong, leg 


extended can be brought to 90* with body. Prom his conver¬ 
sation, one would judge that he had suffered from satyriasis. 

Vision .—No failure to recognise colours, he has recently 
complained of dimness of vision of the right eye. There is com¬ 
mencing optic atrophy, affecting especially the temporal half of 
the disc, and apparently some cupping, vessels normal, the fun¬ 
dus has a gray appearance in this situation, and the vessels are 
curved. There is no myopic crescent. 

Mental condition .—He is able to converse on most subjects, 
and to give an account of his life, which accords fairly well with 
what his wife had told me. He has a fair knowledge of time and 
place, but he has delusions about his wife’s fidelity or her .father’s 
accusations against him on this score. He has moderate gran¬ 
diose delusions about his property, and what he can do when he 
gets out. Prom his conversation he has evidently been leading 



a very loose and extravagant life, throwing his money away at 
music-halls and otherwise ; still, one recognises that in all he says 
there is a certain amount of truth and reason mixed with folly 
and irrationality. 

History (from wife and sister).—Wife had no children ; she 
herself has good health, he was a good, kind, and affectionate 
husband. He suffered for five years with locomotor ataxy. Up 
till six months ago he was mentally quite right, then she noticed 

Fig. 34. 

= Cutaneous Anaesthesia 

he became lustful, irritable, sleepless, given to extravagance, and 
planning all manner of schemes; lately has become suspicious, 
jealous, and at times violent, threatening to murder people, and 
having delusions about his wife’s fidelity. This is indicated in 
the letter which he has written, which shows both dementia and 
delusions, also characteristic tremor, and leaving out of words 



and syllables. His wife noticed that since his mind became 
affected he had become much stronger in his legs . She made this 
remark without any leading question being put. 

March 2, 1901.—He suddenly fell down, Dr. Bolton who saw 
him describes the fit that ensued as follows. Marked clonic 
spasms of the right side of the face, less marked to the left. 
Right arm lying still. Left arm occasionally moved, apparently 
voluntarily as the patient pointed towards his head. Then the 
right arm was convulsed and next the legs, the right being more 
affected than the left, a tonic left-sided spasm then occurred 
followed by clonic movements of the left leg and left arm, and 
later the right leg and right arm. The left arm next became 
straightened out and the left bent at a right angle, the left leg 
flexed and the right leg straight. This was followed by marked 
conjugate deviation of the head and eyes to the left, and the left 
side of the face became more convulsed than the right. Pupils 
measured 7 mm. There was no ataxy noticeable in these move¬ 

April 7, 1902.—Came to the laboratory. Mentally he is much 
freer of delusions. He appears in* better physical health and the 
acute maniacal symptoms which he had on admission, accompanied 
by exaltation, have in great part subsided. He remembered me, 
and conversed fairly intelligibly. There is slight tremor in the lips 
and tongue, and his speech is somewhat syllabic and hesitant. 
He knows how long he has been at Claybury and the day of the 

Physical condition .—He is still very ataxic, walks by the 
aid of a stick, with a wide base; knees extended, head looking 
forward and on to his feet, and stamping gait. Lying flat on his 
back on a couch it was noticed that he had partial footdrop both 
sides , due to weakness of the dorsal flexors; by an effort of 
attention even with his eyes closed he could dorsally flex the foot, 
but if his attention were taken away, the foot would fall back 
again. When told to flex the knee and hip simultaneously, the 
failure of the dorsal flexion was noticeable, when told of it he 
immediately tried to correct it, and this he could do by an effort 
of attention, but it was noticed that the correction did not come 
•till after the flexion of the hip and knee had taken place, and 
an appreciable interval elapsed ; owing to the fact that it was 
brought about entirely by cerebral impulses. 

Sensation (subjective).—He complains of numbness on the 
soles of the feet, and when tested there is manifested some 
hypaesthesia and hypalgesia of the feet on both sides. There is a 



complete loss of sense of position in the toes and ankle joints, 
and also to some extent of the knee-joints. There is considerable 
hypotonus of the hamstrings on both sides. 

Thoracic sensibility .—This seems to have changed somewhat 
since I last examined him. I can now find no definite anaesthesia 
of the left half of the thorax in front, corresponding with the 
anterior divisions of the roots, but over the posterior divisions 1 
find loss of sensibility to light tactile impressions over the fourth 
to seventh segments. The right half of the thorax the same con¬ 
dition obtained posteriorly, but in front a very curious condition 
existed; either he did not feel at all light tactile impressions over 
the front of the chest, extending from the fourth to seventh 
segments, or if he were touched more heavily he invariably 
pointed to a corresponding point on the left side of the thorax, 
(allochiria). These observations were quite reliable. He does 
not now show any hyperesthesia. The epigastric reflexes were 
present on both sides also the cremasteric. The plantar are 
absent, there is no marked incoordination in the hands, but there 
is some loss of sense of position in the joints. There is no im¬ 
pairment of tactile sensibility. The pupils measure, left 6 mm., 
right 5 mm. A week ago he had paresis of both external recti; 
this, however, is now passing off. Three weeks ago he had an 
attack of profuse diarrhoea which Dr. Bolton considered was of 
the nature of an intestinal crisis. 

Patient improved and tried to make himself useful until 
July 15 when he had a succession of seizures which terminated 
fatally in twenty-four hours from commencement. 

Post-mortem notes (abstracted).—Well nourished. Scar in 
region of frenum. Dura mater, intensely congested, other¬ 
wise natural. Subdural spaces.—Great excess of fluid, well over 
tentorium. Pia-arachnoid.—Considerable fronto-parietal milkineas 
and thickening, marked pial extravasations in the poatero inferior 
part of the external surface of the right hemisphere, slight ditto 
left hemisphere. The whole encephalon is intensely congested. 
Weight 1,415 grammes. Bight hemisphere 632 grammes, left 
590 grammes. Left hemisphere more simply convoluted than 
right. Fourth ventricle.—Covered with very fine granulations, 
most marked in calamus. Heart.—Dilated and flabby. 
Valves.—Mitral shows slight atheroma. Coronary arteries.—A 
little early atheroma. Aorta and great vessels.—Marked athe¬ 
roma in all stages, mixed calcareous and pearly fibrosis. 
Abdominal aorta.—Markedly atheromatus. 

Cause of death .—Cardiac failure and general paralysis. 



Microscopical examination (by Nissl method).— Brain , left hemi¬ 
sphere : First frontal. —Marked vascular congestion, perivascular 
lymphatics filled with proliferated plasma cells. Disordered 
Meyert's columns, acute cell changes; glia cell proliferation; all 
cortical layers affected. Vascular changes more marked in the 
deeper layers. Moderate increase of spider cells in superficial 
layers of cortex. Many of the small, and a fewer number of the 
medium sized pyramids, distorted in shape. The cell changes 
appear to be more marked in the polymorphic and granular cells 
of the deeper layers. Coloration of protoplasm of many of the 
cells suggests coagulation necrosis. 

Second frontal .—Changes similar but very much less intense. 
There is obviously an association between the vascular and acute 
cell changes in the first frontal. 

Loiver part of ascending frontal and parietals and Broca. —The 
same changes as above, only more marked. The small and medium- 
seized pyramids are more affected. The perivascular lymphatic 
cell proliferation is very marked, especially in the deeper layers. 
The cells do not present the appearance of experimental anaemia 
produced by ligation of four arteries with recovery, but much 
more the appearance of a coagulation necrosis, such as is pro¬ 
duced by toxic agents, a fatal dose of abrin or ligation of arteries 
without re-establishment of circulation. The protoplasm of the 
cells stains a uniform dull diffuse purplish blue, instead of a bright 
blue. The medium and small-sized pyramids in this respect, 
contrast with the large Betz cells, the majority of which show 
normal Nissl-granules. Pappenheim’s stain shows abundance 
of plasma cells around vessels, and some are found in perineu- 
ronal spaces (vide figs. 3, 5, 6, Plate VIII.). 

Top of ascending frontal .—Very little vascularity and conges¬ 
tion or perivascular cell proliferation. Small and medium sized 
pyramids deficient, much more so in some places than others. 
Betz cells numerous, the majority appear fairly normal. In 
some the nucleus is large, clear, and swollen, others show deficiency 
of chromophilous substance. The small and medium pyramids are 
distorted, and processes broken off. 

Spinal cord. —Naked eye degeneration in usual situation 
and amount of the sclerosis corresponds with the second stage erf 
ataxy in the cervico-dorsal and lumbo-sacral regions. Gray 
matter, lumbo-sacral region ; marked vascular stasis probably asso¬ 
ciated with epileptiform seizures. No great excess of leucocytes 
around vessels or in contained blood. Neuroglia cells, small 
variety in abundance. Ganglion cells of anterior and posterior 
horn, apparently normal in numbers. Anterior horn cells are 



rather swollen (probably acute change from venous congestion), 
nucleus large and clear. Nissl-granules in cytoplasm, and in pro¬ 
cesses fairly abundant and normal in tint and shape. Cells of 
base of posterior horn and substantia gelat. apparently in numbers 
normal. I am unable to judge whether the protoplasm of the 
cells is normal. The slight cell changes that exist are probably 
due to the venous congestion occasioned by the seizures in which 
he died. The glia cells of the degenerated posterior columns are 
mostly small round or oval, there are some few Deiter’s cells more 
than elsewhere, also granulation corpuscles and excess of glia 

Microscopical examination of the central nervous system for 
acute degeneration (by Marchi method).— Cerebrum .—Various 
portions of the brain which were examined by Nissl method were 
also examined by the Marchi method; no recent degeneration 
was found in the superficial layers of the cortex. A considerable 
number of degenerated radial-fibres were found in the ascending 
parietal, but very few in the ascending frontal. This accords 
with the fact that very few degenerate fibres were found in the 
pyramids of the medulla oblongata and in the antero-lateral 
columns of the cord. In the medulla a well-marked degeneration 
was found in both ascending branches of the fifth nerve, there 
was considerable vascular congestion and numbers of black 
points due to degenerated collaterals in the cranial nuclei of the 
fourth ventricle, and the cells of many of the nuclei were stained 
black. That the degeneration of the ascending branches of the 
fifth nerve was genuine was shown by the fact that the adjacent 
restiform bodies were quite free of black particles and granu¬ 
lation corpuscles. 

The spinal cord exhibited very little recent degeneration, but 
the fifth cervical segment showed a number of recently degener¬ 
ated fibres on one side in the postero-external column, especially 
in the cornu-radicular and root zones. This to a less extent was 
seen in the remainder of the cervical segments below the fifth. 
The examination of the dorsal segments showed a marked dilata¬ 
tion of the central canal, normal epithelium lining the whole 
canal, and, therefore, it was a true heterotopia (vide Plate IV.). 
Around the dilated canal were proliferating, round glia cells. Both 
the epithelium cells lining the central canal and the glia cells are 
filled with black granules, products of degeneration, thus showing 
that they have an active phagocytic function. A further descrip¬ 
tion of the epithelial and glia proliferation is given on p. 293. 

Microscopical examination for chronic degeneration (by Weigert 



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Tabes in Asylum and Hospital Practice. 

To face p. 185. 




and Marchi-Pal methods).— The same regions of the brain were 
examined, and a marked atrophy of the tangential and supra- 
radial fibres was found in the ascending frontal and second 
frontal, very much less in the ascending parietal. There was 
complete loss of these fibres in the orbital and prefrontal convo¬ 
lutions, and in these regions there were a large number of 
branching glia cells. 

Spinal cord .—There was very marked degeneration of the 
root fibres and their intramedullary projections extending from 
the fourth cervical downwards to the termination of the cord, but 
the degeneration was most advanced in the lumbo-sacral and 
mid-thoracic regions. The endogenous fibres were in this case 
markedly affected, there was a great diminution of the fibres of 
the comma tract, the posterior internal zone, septo-marginal 
tract, and the oval area of Flechsig, likewise the small median 
triangle of the sacral region. A considerable number of fibres 
have disappeared from the cornu commissural zone and been 
replaced by glia tissue, but this portion of the posterior column is 
the least affected. Owing to the heterotopia in the dorsal region, 
the course of the endogenous fibres can be more distinctly seen 
than in other spinal cords of an equally advanced degree of tabes, 
with posterior column atrophy and sclerosis. Fibres can be 
distinctly seen passing from the base of the posterior horn round 
Clarke’s column to form the posterior commissure, decussating 
with similar fibres from the opposite side. These fibres are of 
endogenous origin, as they are of fine texture, and can be seen 
starting from the region mentioned, while the fibres of the root 
zone are entirely absent, and therefore cannot give origin to 
them (vide fig. 2, Plate IV.). 

Teased preparations of the posterior roots attached to the 
third, fourth, fifth, sixth, seventh, and eighth cervical segments 
were made. The root-fibres of the third segment were mostly 
small or medium-sized medullated fibres; they showed no 
neurilemmal nuclear proliferation. The roots of the fifth showed 
a number of large medullated fibres with well-developed myelin 
sheath, and no nuclear proliferation, but there were also a large 
number which showed the myelin sheath in various degrees, 
attenuated, and these exhibited a marked nuclear proliferation of 
the neurilemma. Again, in some there was complete absence of 
the myelin, and apparently only the neurilemma, the cells of 
which had undergone marked proliferation, was left. Below 
this level the rootlets contained only a few solitary myelinated 
fibres, and in these the sheath was much attenuated. 


Case 47.— Tabo-paralysis , grandiose delusions , ataxy. Duration 
of disease said to be one year. 

W. J. W. Occupation, labourer. Aged 31. Admitted to 
Claybury Asylum, November 18, 1895, under the following 
certificate: “ He is strange in bis manner, and varied in his 
moods. At one time he is depressed and pre-occupied, and at 
another laughs, sings, and whistles. Declares he is a great 
fighting man, and states that he is the possessor of a gold belt 
worth £11,000, awarded to him for his successes as a pugilist. 
He also asserts that he has been a soldier in India, and has fought 
many battles, and has obtained three medals for the same 
(although I am informed that he has never been abroad). He 
further tells me that he is going to buy some land and build 
houses upon it, which he proposes to let free of charge to the 
poor. He is wet and dirty in his habits, and his memory is 
is impaired/* 

Condition on admission .—Pupils equal. A. B. irregular, gait 
ataxic, knee-jerks abolished. Scar on penis. Symptoms com¬ 
menced seven months before admission, probably the cord 
symptoms of longer duration. 

Mental condition .—As above. He is irrational and incoherent. 

December 7, 1895.—He is noisy night and day, very mis¬ 
chievous, pulls himself up by the blind cord. Grandiose delusions 

January 15, 1896.—Advanced general paralytic. He has had 
one or two slight seizures. He is very paretic, and in poor 
general health and condition. 

February 8, 1896.—Died of exhaustion of general paralysis. 

Autopsy .—Convolutions of the brain are well formed, and are 
not wasted ; the pia-arachnoid is slightly thickened, but it is not 
adherent to brain substance. Lateral ventricles are normal, the 
fourth is dilated and slightly granular in its lower part. The 
posterior columns of the spinal cord are wasted; the aorta is 
slightly atheromatous at its base. There is hypostatic congestion 
of the bases of both lungs. On the penis there is an old scar. 

Microscopical examination .—First frontal convolution showed 
some early changes characteristic of dementia-paralytica. The 
tangential and supraradial fibres were greatly diminished, some 
increased vascularity, atrophy and changes of the superficial 
pyramidal cells, and distortion of Meynert’s column. 

Spinal cord .—The cervical, thoracic, and lumbo-sacral regions 
showed advanced sclerosis and atrophy of fibres in the usual 
situations. There is some atrophy of the endogenous systems, 



the least to be affected being the cornu commissural zone. The 
posterior roots are markedly atrophied, only a few myelinated 
fibres being left in the lumbo-sacral regions {vide fig. 39). In the 
lateral and anterior columns there are diffuse scattered de¬ 
generated fibres, but there is no sclerosis. There is marked 
vascular congestion throughout the cord and medulla. In the 
sclerosed areas there is an obvious thickening of the vessel walls. 
The appearances of the cord lesions would indicate tabes of some 
years standing. The notes which are taken from the case book 
are too brief to be of much value. 

Case 48.— Tabes of four years' duration, onset of mental symp¬ 
toms of general paralysis, admission to asylum, epileptiform 
seizures, attacks of vomiting, death about one year later. 

W. T., aged 38, single, tinsmith, under the care of Dr. Head, 
to whom I am obliged for allowing me to make an abstract of 
his notes. Admitted to London Hospital June 5, 1897. 

Personal history. —Chancre at 22, which ate away the frenum, 
followed by repeated ulcerated throats, noticed no rash. He has 
had pains in his legs and stomach for eighteen months. Last 
year he had double vision, which lasted six months before it 
began to improve. Very tired when walking, no difficulty with 
his bladder, except that he cannot hold his water so long as he 
used to be able to. About eighteen months ago he became lust¬ 
ful, very different from what he had been before. He had plenty 
of power, but for the last six months he has become very feeble, 
but desire is still present, but erection fails. No trouble with 
the rectum, or other illnesses. He has always earned good 
wages, has drunk a good quantity, but never enough to incapaci¬ 
tate him. There is nothing noteworthy in his family history, 
with the exception that one brother is asthmatic. 

Nervous system. —Speech good, no attacks or fits, no head¬ 
ache, stands perfectly steady, with the feet together and the 
eyes open. With his boots on and his eyes shut, no swaying 
movement is noticed, but these come on when he takes his boots 
off. He can rise from toes to heels quite easily with bis eyes 
open, but he tends to fall forwards when his eyes are closed. 
Very slight incoordination of left hand, with eyes shut on touch¬ 
ing the nose, no paresis. He complains of rheumatic pains in 
both knees, a tired, aching feeling, but not shooting pains. 
Cutaneous sensations in all forms both in time and place are 
excellent. Knee-jerks are present on both sides without reinforce¬ 
ment, the right greater than left. On a previous occasion the left 



could not be obtained without reinforcement. Plantar and ab¬ 
dominal reflexes good. Pupils equal, 2 mm., Argyll-Robertson 
phenomenon. Paresis of right external rectus. Face movements 
good, no tremor of tongue, sphincters normal. Perimeter tracings 
showed considerable concentric limitation of field of vision. He 
attended as one of Dr. Head’s out-patients until June 24, 1899. 
He then disappeared, and was admitted into Bexley Asylum. 
When I saw him he was suffering with symptoms of general 
paralysis. The speech was slightly slurred, the tongue tremulous, 
also the face muscles; there is an expression of mild exaltation, 
but he is able to answer questions and give a history of his 
occupation and illness which corresponded fairly well with the 
account contained in Dr. Head’s notes. There is, however, some 
defect in his knowledge of time and place, but no pronounced 
delusions were discoverable. He now has some bladder trouble, 
diminished sensation to pain in the lower extremities; the trunk 
was not tested, muscular hypotonus in addition to the symptoms 
of ataxy previously noticed. He became progressively more de¬ 
mented, but rather tended to childishness than absolute loss of 

On October 12, 1900, he commenced having epileptiform 
seizures, and he was found by Dr. Piper convulsed on both sides 
and in a state of opisthotonus, his temperature was 102°, and he 
was sweating profusely. He was first in a comatose and after¬ 
wards in a semi-comatose condition. He had a large number of 
seizures of a similar character, but affecting especially the left 
side, and on October 15, it is noted that he had twenty-two 
seizures since October 12. 

October 22.—It is noted that his tactile sensation was tho¬ 
roughly tested, no alteration was detected, and there was certainly 
no hemianaesthesia present. The note further states he is now 
quiet, and can answer intelligently when spoken to. His memory 
is considerably impaired, and he often becomes confused in con¬ 
versation. He passes his water naturally, and has control of his 
motions. No important change occurred, but progressive mental 
and bodily enfeeblement until February 9, when he commenced 
having a series of convulsions, and it is still noted that there is no 

On February 28, he commenced having attacks of vomiting, 
which continued for more than a week, associated with retention 
of urine, which persisted after the vomiting had ceased. 

On March 21, the notes state “he was transferred yesterday 
to the general paralysis infirmary for the purposes of better classi- 


(1) (2) (3) (4) 

Photomicrograph of strips of the brain which are from left to right. (1) Small and 
medium sized pyramidal layer, top of ascending frontal, showing abolition of Meynert’s 
columns produced by destruction and distortion of the pyramids. Not a healthy cell is 
seen. There is a marked proliferation of glia cells. (2) The same section of the cortex 
in the deeper layer of large pyramids. Two Betz cells are seen together, one is obviously 
destroyed and has been partially devoured by phagocytes. Most of the cells are 
abnormal. (3) Pyramidal layers of occipital cortex. Both as to numbers and conform¬ 
ation they present a comparatively normal appearance. (4) Broca’s convolution. Very 
marked destruction of medium sized pyramids shown. 

To face p. 189. 



fication.” He is still sick at intervals; mentally he is very 
demented, but quite happy. He vomited at intervals up to his 
death on April 6. 

Post-mortem examination. —Showed little in the organs of the 
body except in the brain and spinal cord, but it may be noted 
that there was an old calcareous nodule at the apex of the left 
lung, some emphysema of both lungs, a moderate amount^of 
atheroma of the aorta, and considerable chronic cystitis. 

Brain .—Weight of right hemisphere, 518 grammes; weight of 
left hemisphere, 542 grammes. Granulation of the third and 
fourth ventricles, dilatation of all ventricles, left lateral ventricle 
less than the right. Pia-arachnoid adherent in pre-frontal region 
mid-line, leaving erosions on stripping. External appearances of 
hemispheres.—Eight: Obvious wasting of base of first frontal and 
base of inferior frontal at junction of acending frontal. Left: 
appears less wasted as a whole, but there is a small triangular 
depression due to atrophy just above the angular gyrus : appear¬ 
ance of gray matter of cortex is somewhat wasted, but wasting 
is not universal. Striation in many places indistinct. Same 
applies to right side. 

Notes of the microscopical examination of the central nervous 
system.—Nissl staining of the cortex. —The small and medium 
sized pyramids show their processes broken off; the apical 
processes are either not present or cork screw. The cyto-plastn 
stains diffusely and imperfectly; the nucleus is often eccentric. 
The columnar arrangement of the cells of Meynert’s layers has 
disappeared. The small cells of the molecular layer and the small 
pyramids are especially affected in the first frontal, ascending- 
frontal, ascending-parietal, and Broca’s convolutions, but to a less 
degree in the occipital. The large Betz cells of the ascending 
frontal occur in groups, some of which appear quite normal, others 
show chromolytic changes, swelling of nucleus, and breaking off of 
processes, and some exhibit excess of yellowish pigment. 

The medium and small-sized pyramids are much more affected 
in these regions than in the occipital lobe {vide Plate V.). 

As a rule the vascular changes are not pronounced, but many 
small veins in all regions of the cortex show, the perivascular 
lymphatics filled with basophil staining cells ; there is not excessive 
glia cell proliferation. 

Spinal cord, stained by Weigert method (each segment being 
examined)—Cauda equina and fifth sacral. All the posterior 
roots are atrophied, and almost totally denuded of fibres; some 
few atrophied myelinated fibres can be seen in some of the roots. 



The vessels are congested, but the walls are not thickened, and 
they are obviously distended with blood merely from ante-mortem 
stasis, for the anterior roots, which are quite normal, contain 
vessels similarly gorged with blood. Third sacral and roots.— 
Roots same as above. Posterior column sclerosis, and almost 
complete denudation of fibres, except in area corresponding to 
the anterior two-thirds of the portion of the posterior column 
surrounding the posterior median fissure ; behind this up to the 
periphery there are scattered fibres corresponding, doubtless, to the 
endogenous fibres belonging to the oval area of Flechsig. Second 
sacral and roots.—Posterior roots markedly degenerated, but 
contain some fibres (large) undegenerated. The whole posterior 
column is partly denuded of fibres, except the median oval area 
and the cornu commissural zone. The degeneration is most marked 
in the root zone, and in the zone between the two undegenerated 
endogenous tracts (fibres of GolTs column). Crossed pyramidal 
tracts, both sides degenerated. First sacral.—The roots are 
entirely devoid of fibres, and the whole of the posterior column 
is sclerosed and denuded of fibres. The cornu commissural 
zone and oval area are the only tracts which contain fibres, 
and here they are relatively abundant. Fifth lumbar.—Posterior 
roots not nearly so much affected as first sacral, roughly 
speaking, quite one-third of the fibres still left. Degeneration 
in the same regions as the last, but a proportional increase to 
the numbers in the roots of fibres entering the posterior 
columns. Fourth lumbar.—Ditto, with regard to fibres in roots, 
except the two endogenous tracts are being separated by the 
degenerated areas corresponding to a tract which intervenes and 
approximates at the middle line, separating thus the fibres of the 
oval area, which are pushed backwards, although there are still a 
number of fibres scattered in the degenerated area. The crossed 
pyramidal tract is seen to be more degenerated in the left than the 
right side; the posterior column degeneration is about equal on 
the two sides, and in the median line extends forwards to the 
posterior commissure. Third lumbar.—Ditto, atrophy of fibres 
of the posterior roots, otherwise the same as fourth. Second 
lumbar.—Ditto. Here is seen commencement of Clarke’s column, 
and there is some atrophy of the entering roots and of the fine 
plexus, but it is not marked. There is less atrophy of fibres of 
the posterior roots. First lumbar.—Ditto, but the atrophy of the 
feltwort of fibres around the cells of Clarke’s column is very 
evident as the column is more developed ; the encircling tracts of 
endogenous fibres are, however, relatively abundant. Twelfth 



dorsal.—Boots much smaller, less number of degenerated fibres, 
yet very marked atrophy of fibres entering Clarke’s column, and of 
the plexus of fibres ; most marked degeneration in root zone and 
area extending thence to mid line ; slight degeneration of Lissauer’s 
tract, moderate of postero-external triangle. Eleventh dorsal.— 
Posterior roots much less affected. Less atrophy of root zone and 
of fibres entering Clarke’s column, also of other short tracts, e.g ., 
Lissauer’s. Tenth dorsal.—Ditto ; attached roots show very little 
degeneration. Ninth dorsal.—Boots of one side almost denuded 
of fibres, and the postero-external column and posterior horn of 
the same side considerably shrunken. Eighth dorsal.—Ditto. 
The crossed pyramidal sclerosis is becoming less obvious, and 
above this level is no longer recognisable by the naked eye, 
although microscopically a little diffuse sclerosis can be found 
on one side as high as the sixth dorsal. Seventh dorsal.—The 
posterior roots are partially but equally affected on both 
sides. Lissauer’s tracts are very little affected at this level. 
Sixth dorsal.—The posterior roots are much more affected on 
the right side than the left. Fifth dorsal.—Boots completely 
atrophied both sides; both coarse and fine entering-fibres dis¬ 
appeared. Fourth dorsal.—Ditto. Third dorsal.—Boots atrophied 
both sides, one side more completely. Second dorsal.—Ditto. 
First dorsal.—The roots now contain a considerable number of 
healthy fibres, and the cornu radicular zone and the entering 
zone of Lissauer show very little sclerosis ; still there is a great 
amount of atrophic sclerosis in the posterior columns owing 
to the atrophy of long and medium length fibres proceeding 
from lower levels, and although there is no posterior root 
degeneration above this level, it is not until we reach the seventh 
cervical segment that the sclerosis in the root zone entirely 
disappears. Eighth cervical.—Not much degeneration of root- 
fibres, cornu radicular and Lissauer’s zones almost free of 
sclerosis. Seventh cervical and upwards.—The roots are healthy, 
and two well-defined tracts of sclerosis are seen, one overlapping 
the triangle of Goll’s column, but a healthy strip intervening. We 
have seen that the roots of the lowest lumbar and sacral regions 
were almost devoid of fibres, and I have shown experimentally 
that nearly all the fibres of this triangle of Goll’s column come from 
the fourth and fifth lumbar and first and second sacral roots, which 
were, correspondingly, in this case the roots especially atrophied. 
Above this level, up to the ninth dorsal, the roots contained a large 
number of healthy fibres ; we must, therefore, accord to this 
narrow, undegenerated A-shaped strip an origin from these roots. 




Fig. 35. 

Drawing made 
with Edinger appa¬ 
ratus. Black part 
indicates complete 
or very extensive 
sclerosis. Dots indi¬ 
cate partial de¬ 
generative sclerosis. 
It will be observed 
that the eighth and 
ninth segments show 
a marked degenera¬ 
tive atrophy of the 
roots and posterior 
column on one side. 
Possibly this may be 
associated with the 
gastric crises. 

♦The degeneration 
of the crossed pyra¬ 
midal tracts is not 
so complete as the 
above would indi¬ 



and they convey, in all probability, kinaesthetic impressions from 
the large muscles connecting the trunk and legs and the lower 
part of the trunk. At the level of the second cervical we have in 
front of this a A-shaped area of degenerative sclerosis, which 
corresponds to the outfall of the root-fibres in the upper dorsal and 
lowest cervical regions; here again it is certain that these fibres 
belong especially to* the segments of the cord conveying kinaesthetic 
impressions from the small muscles of the hands, viz., eighth 
cervical and first and second dorsal, for I have shown experi¬ 
mentally that the greater part of the fibres which* form this portion 
of the cerebro-petal kinaesthetic tract come from the eighth 
cervical and first dorsal segments, which we know innervate the 
small muscles of the hand. 

In front of this at the level of the second cervical, the healthy 
fibres of the roots entering the cord in the cervical region, and on 
their way to the postero-external nucleus (Burdach’s) have taken 
up their position in the form of a A, the limbs of which at their 
base are continuous with the root zone. 

The A-shaped strips of fibres coming from fibres of the 
posterior roots are segmental, each root sending a certain number 
of fibres which take up a position lapping over the last, and, as we 
have seen, the number of fibres which each root provides is 
distinctly proportional to the complexity and variety of move¬ 
ment of the structures innervated, thus the great bulk of these 
fibres, viz., the fourth and fifth lumbar and the first and second 
sacral which innervate the muscles of the feet, the eighth cervical 
and first and second dorsal, which innervate the small muscles 
of the hand come from the mobile apices of the limbs. Sherring¬ 
ton has shown that from above downwards in the cerebral cortex 
there is spinal segmentation of the efferent path to the muscles 
in the motor area of the ascending frontal. Here in the posterior 
column we have a spinal segmenation of the afferent kinaesthetic 
path, and just as the greater part of the upper two-thirds of the 
motor area is concerned with the complex movements of the 
hand and foot, so the greater part of the kinaesthetic path to the 
cerebral cortex is concerned with conveying impressions from the 
hand and foot. 

Association of morbid anatomical conditions with symptoms .— 
(1) The advanced and unusually pronounced degeneration of the 
lowest sacral roots—early impotence. (2) The presence of fibres 
in the posterior roots of the third and fourth lumbar segments in 
addition to the crossed pyramidal degeneration on both sides, but 
more marked on one side—the knee-jerks present on both sides, 




but greater on the right than the left. (3) The obvious atrophy 
of the posterior horn in the seventh and eighth segments on one 
side with shrinking of the cord (as in Case 31)—the existence 
of gastric crises. (4) Atrophy of the tangential, supraradial fibres 
and molecular layer, small and medium sized pyramids, especially 
of the frontal and fronto-centrai regions—progressive dementia. 
(5) Slight vascular changes, little glia cell proliferation—no pro¬ 
nounced maniacal symptoms or delusions. 

Case 49.— Tabic * amyotrophy. Tabes affecting especially the arms 
followed by muscular wasting of small muscles of hands . 
Seven years' duration , commenced with optic atrophy and 
terminated with mental symptoms and convulsions . Post¬ 
mortem examination.—Wasting of hemispheres , especially the 
right , granular ventricles , other naked eye and microscopic 
characteristics of general paralysis . The cord exhibited the 
usual appearances of advanced tabes , but also atrophy of 
anterior horn cells in lower cervical and upper dorsal regions , 
also atrophy of cells of Clarke's column tuith degeneration of 
ventral and dorsal cerebellar tracts . 

A. J., aged 42, single. Admitted to Marylebone Infirmary, 
May 1, 1894. For the last thirteen years, parcel-post sorter, 
previously a soldier. History of a buboe ten years previously. 
Fifteen months ago eyesight began to fail, drooping of the left eye¬ 
lid, double vision, and things appeared smaller than natural. He 
also suffered with attacks of giddiness, lightning pains, and later 
weakness in the legs which prevented him walking. 

The following notes were taken on admission. —Left eye, external 
strabismus, pupil half the size of that of right, can only just 
appreciate light with this eye. Right-eye movements to right 
made with difficulty. He cannot distinguish objects on the right 
side of him. Pupil much dilated. Nystagmus in both eyes in 
upward and downward direction. Both pupils are said to react to 
light and accommodation. The arms.—No apparent wasting, 
muscular power good, great loss of coordination in both arms, deep 
reflexes cannot be obtained ; complains of numbness in hands, but 
sensibility to touch seems normal, sensibility to heat and cold also 
normal. Legs.—Muscles feel flabby, patient says his legs are 
much thinner than they were. Knee-jerks absent; sensation 
normal. On trying to walk patient staggers helplessly. Taste.— 
Can distinguish between hot and cold, salt and sweet, but is very 
slow in distinguishing flavours. Bladder normal, no incontinence. 
Speech natural. September 0, 1894. Seen by Dr. Beevor who 



found muscular sense very much impaired. Sensation to touch in¬ 
definite. No loss of tactile sensation in legs. Muscular sense 
much impaired. Wasting and loss of power in thumb muscles. 
November 19, 1895. Small muscles of the left hand give no 
reaction to faradic current. Small muscles of the right hand 
thenar, hypothenar and interossei require a stronger current than 
normal to give the faradic reaction. Sensation to touch is blunted 
on chest and arms, no loss of sensation to heat and cold. On 
moving the fingers the patient can tell which fingers are moved, 
but is unable to state what the movement is. Incomplete loss of 
muscular sense. Eyes.—Marked nasal hemianopsy still present. 
Eight pupil does not react to light or accommodation, the left reacts 
to accommodation, but not to light. Loss of sensation to touch in 
both legs, but no analgesia over legs. 

1899.—Examined by Dr. Beevor. Partial anaesthesia found in 
legs, localisation very poor. Very little tremor in the facial 
muscles. Patient now has power in the biceps and deltoid muscles 
of the left arm, and can flex and extend fingers. He has periodic 
attacks of exaltation. 

May, 1900.—Analgesia in both upper extremities, anaesthesia 
on both sides up to clavicle, including arm. 

On November 6, 1900, he was first seen by me, and I made 
the following notes. He is now semi-delirious, and not in a fit 
state to test sensation. On Sunday last, November 4, he had a fit, 
cried out, and lost consciousness for two minutes. A good deal of 
twitching, convulsive in character, took place on the left side, arm, 
leg, and face, and this lasted for twenty-four hours. He has not lost 
consciousness since then. Previous to this attack patient was 
noisy and sullen, but had no delusions. Since the attack he has 
seen people coming into the room and called out to them saying 
they were robbers. He has not refused food since fit, or had 
delusions about same. Since Sunday night he has suffered 
with vomiting and reaching and also hasmatemesis. Patient has 
no personal illusions. Nearly blind, right pupil 5 mm., left 4*5 mm. 
Inactive to light. Slight ptosis, more marked on right side, and 
partial immobility of right globe. He cannot be made to look 
when testing vision, being nearly blind in left eye, seeing best with 
right eye. Notes state that there is optic atrophy and hemiopia. 
Appetite has been ravenous. There is a little apparent loss of 
expression on the right side of face. Tongue very tremulous, 
characteristic of general paralysis, but no tremor of lips, or any 
speech affection. His lower extremities are very wasted, especially 
the dorsal flexor group of muscles of the front of the legs, both 



the peroneal group, as well as the tibialis antieus and long exten¬ 
sors of the toes; there is talipes equino-varus in consequence, and 
the toes are plantar flexed; he does move legs, according to the 
nurse, but only in an incoordinate manner. There is marked 
wasting of the interrossei and muscles of thenar and hypothenar 
eminences, especially of the left hand. He moves right hand but 
not fingers much more than the left, but then only in a most in¬ 
coordinate manner. He smells ether but not peppermint. He 
was not in a fit mental state to test sensibility, but apparently he 
felt pricking with a needle on the legs, as he swore violently. 

The patient died January, 1901, and by the kindness of 
Dr. Lunn the brain and spinal cord and many of the peripheral 
nerves were forwarded to me for examination. Unfortunately the 
cord was somewhat damaged in several regions, so that an abso¬ 
lutely complete examination of this interesting material could not 
be made. 

Brain .—Pia-arachnoid thickening, especially over frontal and 
central convolutions. Eight hemisphere smaller than left, and more 
atrophied. Marked dilatation of lateral ventricle. Ependyma 
granular, marked granulation of ependyma of fourth ventricle. 

Microscopical examination (Marchi method).—Left Broca, no 
recent degeneration. Eight ascending frontal and parietal and 
base of second frontal, a number of recent degenerated radial 
fibres, especially in the two former gyri. Sections of the same 
convolutions at the level of the base of the first frontal showed 
not nearly so many degenerated fibres. Left hemisphere, results 
similar. Orbital lobe and olfactory nerves showed no recent 

Marchi, Pal, and Wolter’s methods.—The same convolutions 
were examined. First and second frontal.—Tangential and supra- 
radial fibres absent; interradial diminished. Ascending frontal. 
—Tangential and supraradial fibres partly diminished; inter¬ 
radial diminished. Ascending parietal.—Tangential and supra¬ 
radial absent; interradial diminished. Broca.—Tangential and 
supraradial greatly diminished. First temporal.—More tangential 
and supraradial fibres than in other regions examined. Orbital. 
—Superficial fibres are diminished. Both optic nerves and tracts 
show very complete atrophic degeneration as far as geniculate 

Nissl method .—All the above regions of the cortex were 
examined, and showed marked congestion of vessels, and plasma 
cells in perivascular lymphatic sheaths. The cells of the 
deeper layers of the cortex present a fairly normal appear- 



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iance, in spite of the marked vascular changes. The outline 
of these cells is well defined, and their apical processes 
straight. The columns of Meynert are fairly well defined. The 
nearer the surface is approached the more numerous $re the 
atrophied and altered cells, processes being broken off and no 
longer retaining a pyramidal form, staining imperfectly and showing 
changes both in the nucleoplasm and cytoplasm. The existence 
of a cell is often only determinable by the persistent stainable 
nucleolus. The glia cell proliferation is slight in proportion to the 
vascular congestion and the cellular decay and destruction. f The 
vascular changes are as marked in the deeper layers as in the 
superficial; the cell proliferation in the perivascular sheaths is 
mainly due to lymphocytes. The vascular and cell changes were 
.much less obvious in the calcarine region. It was concluded that 
the cell change in the superficial layers was for the most part 
primary and chronic and independent of the vascular, which was 
acute, and coincident with the attack of acute mania which had 
supervened a few months prior to death. 

Spinal cord .—(Nissl method). Sixth, seventh, eighth cervical, 
first, second, and fourth and tenth dorsal, first and fifth lumbar 
and first and second sacral examined. Sixth cervical.—No 
atrophy of anterior horn cells. Seventh cervical.—Partial atrophy 
of the anterior and internal groups of anterior cornual cells, the 
lateral groups being normal, or nearly so. Eighth cervical.—There 
is marked atrophy and disappearance of the ganglion cells of the 
anterior horn of the left side, and on the right side the cells are 
greatly diminished in numbers. Many of them have but few pro¬ 
cesses, the Nissl-bodies are absent or diminished, their sides convex 
instead of concave, greatly diminished in size, and in many in¬ 
stances the cytoplasm appears to be filled with yellow pigment 
granules. First and second dorsal:—There is hardly a ganglion 
cell to be seen on either side in the anterior horns. On the right 
there are a few cells in the lateral horn, but these are mostly 
degenerated. Not only is there a disappearance of the anterior 
horn cells, but also of the more numerous smaller cordonal cells 
of the gray matter. There is not a great excess of glia cells but 
large, thin-walled, dilated veins due to the distension of pre¬ 
existing vessels were observed, but no old or recent haemorrhages. 

In the lumbo-sacral region the anterior horn cells show chronic 
atrophic degeneration similar to, but less advanced than that in 
the cervico-dorsal region. There is also atrophy of the cordonal 
cells of the gray matter at the base of the anterior horn and 
throughout the posterior horn. 



Sections of cervical, dorsal, and lumbo-sacral regions stained 
b*y Marchi method exhibited scattered degeneration of recent 
character in the antero-lateral tracts, especially the crossed pyra¬ 
midal ; also a little in the posterior columns in regions corre¬ 
sponding to the cornu commissural zone, where practically fibres 
only exist. 

Examination of the spinal cord by Weigert and other methods 
exhibited a marked degenerative atrophy of all the posterior roots 
and the exogenous fibres of the posterior columns of the spinal 
cord, without any marked vascular change to account for the 
same. The membranes were not much thickened. A consider¬ 
able substitutive overgrowth of glia tissue exists in the posterior 
columns, so that they are not so much shrunken as is often the 
case. Shrinkage of the spinal cord generally to the size of that of 
a child in the first and second dorsal, fifth lumbar and first sacral 
regions, atrophy of the root zone in these regions and of the 
anterior roots was observed. With the exception of a few fibres 
in the cornu-commissural zone close up to the posterior com¬ 
missure (vide Plate VII.), the whole of the endogenous system of 
fibres are destroyed. Probably this may be associated with the 
destruction of the cordonal cells above noted. There is a 
marked atrophy of the fibre plexus of the column of Clarke, 
and an atrophy of the cells at all levels which accounts for the 
partial atrophic sclerosis of the ventral and dorsal cerebellar 
tracts, especially the former. There is also at all levels an 
atrophy of the cells of the posterior horn accounting for the disap¬ 
pearance of all the descending endogenous fibres and a great part 
of the ascending (vide Plate VII.). There is marked flattening 
and shrinking of the cord in the cervico-dorsal region; the 
posterior columns have in this situation, but nowhere else, a 
concave instead of a convex external border, indicating long¬ 
standing atrophy and shrinkage. 

A considerable portion of the dorsal spinal cord had been 
damaged in its removal, and therefore was not of much use for 
examination, but in the light of Purves Stewart’s case of crush of 
the cord in the lower cervical region, with descending degenera¬ 
tion in the comma tract, continuance of the same into the posterior 
external triangle, septo marginal, oval area, and median triangle 
of Phillipe (all the fibres of which are completely absent 
in this cord), and of the fact that there is definite evidence 
of shrinkage of gray matter and disappearance of cordonal cells 
in the lumbo-sacral and cervico-dorsal regions, the following 
facts —(1) atrophy of small muscles of hand and foot, (2) 




atrophy of anterior horn cells in cervico-dorsal and lumbo¬ 
sacral regions, (3) atrophy of gray matter and cordonal cells in 
the region of outflow of nerves to hand and foot, (4) atrophy of 
endogenous systems of cordonal cells and intercalary neurons— 
show reason for the argument that not until there is atrophy of 
the intercalary neurons and of the cordonal cells, which give 
off fibres associating different segments, will the anterior horn 
cells be deprived entirely of stimulus, and, therefore, undergo 
regressive atrophy. Destruction of the exogenous systems alone 
will not suffice, as I have found by cutting a number of posterior 

In the lumbo-sacral region, where the muscular atrophy was 
not so advanced, nor the cell atrophy of the anterior horns, the 
primary nonvascular origin of the process was evident. 

I look upon the morbid processes which occurred in this extreme 
case in the following order : (1) Degeneration of posterior 

spinal afferent neurons. (2) Degeneration of their association 
neurons. (3) Degeneration of intercalary neurons, resulting in 
cutting off completely the stimulus from anterior horn cells, for 
Schafer has shown experimentally that Von Monakow was 
correct in his assumption that the crossed pyramidal fibres 
probably do nob directly arborize with the anterior horn cells. 
(4) Regressive atrophy of the anterior horn cells now deprived of 
all stimulus, and as a result of this, degeneration of the motor 
fibres and muscular wasting. Slight degeneration was found 
also in the pyramids of the medulla, and the crossed and direct 
pyramidal tracts in the spinal cord. Dr. Purves Stewart has 
advanced as an argument against the neurone theory the fact that 
in his case of crush of the cervical cord he has found degenera¬ 
tion in the internal arciform fibres, and, therefore, the degeneration 
has not been confined to one neuronic system. This to my mind 
is full of fallacy, for such a severe lesion as a crush of the cord 
might well give rise to signs of Marchi degeneration (far removed 
from the seat of the lesion) from vascular disturbances and other 
causes. I have had considerable experience in examining the 
medulla after section of the posterior roots, and I have never 
observed, even after cutting all the posterior roots of one side sup¬ 
plying the upper limb with sensation, any degeneration in the 
internal arciform fibres and fillet. I have examined now the 
cords of twenty-eight cases of tabes and tabo-paralysis, and 
even in such extreme posterior column degeneration as this 
case presents, I have never seen any atrophy of the internal 
arciform fibres, although there is complete fibre plexus atrophy 



of Goll and Burdach's nuclei. In refutation of this statement of 
Purves Stewart I call the attention of my readers to Plate VII., 
fig. 1, showing the condition of the internal arciform fibres as 
they leave the posterior column nuclei to decussate in the mid 
line to form the fillet. 

Another fact worthy of note in this case is the existence of 
some fine fibres in the roots of the cauda equina, and also the 
entering rootlets of the lumbo-sacral spinal segments. These fibres 
belong to the external group of fibres, and break up immediately 
into fine collaterals around the neurons of the substantia gelatinosa. 
According to Bechterew they subserve cutaneous sensibility. 
When the sections of the spinal cord were stained by Bolton's iron 
alum method these fibres were seen fairly numerous in some 
sections, whereas the inner group of coarse fibres are entirely 
absent in the roots and in the cornu radicular zone. We can 
associate this anatomical finding with the fact that the patient 
was apparently aware of rough pricking of his legs when I tested 
him, although he was completely helpless and almost blind. 

The ulnar nerves hardly contained any fibres, the nerve was 
shrunken, and the fasciculi consisted mainly of thickened epi-peri 
and endoneurion. The median was only slightly affected, and the 
musculo-spiral not at all. The sciatic nerve was, like the other 
nerves, much smaller than natural; microscopically all the bundles 
showed a marked outfall of fibres, but the atrophy was not nearly 
so marked as in the case of the ulnar nerve. 

This quite agrees with the clinical history of the affection 
commencing in the arms, and of the paralysis affecting the small 
muscles of the hands. 

Case 50.— Tabo-paralysis, ataxy of some standing . Attack of 
mania , grandiose delusions and progressive dementia , death 
six months later. 

J. H., occupation bedstead packer, using a treadle all day 
long, admitted to Cane Hill, September 20, 1901, aged 39, from 
Shoreditch Infirmary. No family history of insanity or nervous 

Physical condition .—Irides blue, pupils in faint light, right 3£, 
left 2f, accommodate to 2£ and 2 mm., strain accommodation, 
equal, 2 mm. No reaction to light, both somewhat irregular, 
especially the right. Extremely marked tongue and jaw jerk, 
patient cannot satisfactorily protrude his tongue owing to the jerk. 



Speech very slow and drawling, with considerable slurring, and at 
times such marked hesitation that it is impossible to make out 
what he wishes to say. Marked tremor of lips. Left upper 
abdominal reflex absent, the others normal. Scar of a stab to 
the left of the xyphoid cartilage and a hole through into the 
abdomen which readily admits the finger. Patient says that it 
was done by his wife with a butcher’s knife. Sensation is delayed 
(both touch and pain) over the abdomen (which is retracted) and 
chest to about two inches above the nipples, and on the front of 
the chest up to this level there seems to be a condition almost of 
analgesia. The results are, however, unreliable owing to the 
mental condition of the patient. The heart is normal. There are 
signs of old consolidation of the apex of the left lung. There are 
several papery scars on the legs, one of which above and inside 
the left knee is markedly serpiginous in outline. The knee-jerks 
are absent, patient feels touch and pain, but has no true plantar 
reflex. If either touched or pricked on the soles of his feet, he, 
after a considerable latent interval, rapidly withdraws the leg, 
wriggles in bed, and complains bitterly of being hurt. Hypotonus 
to 15° beyond a right angle, arm reflexes absent, right grasp fair, 
left grasp very strong. Patient cannot support himself on his 
legs without help. On trying to walk, there are extremely marked 
ataxic movements of the legs, with stamping of the heels ; Rom¬ 
berg sign is well marked. There is a marked scar (patient says 
of a “chancre”) on the left side of the corona on the under 
surface of the foreskin. Patient volunteers the information that 
he has had “ syphilis.” 

General condition .—Patient is a very feeble and emaciated 
man, who is unable to walk or attend to his own wants. He is 
at present somewhat drowsy owing to his having had a powder 
administered yesterday evening. This was given owing to his 
extreme restlessness, lest he should be injured by throwing him¬ 
self about. During examination patient either replies drowsily 
to questions or is restless and groans. He complains of pains in 
his “ body, and legs, and all over.” No more definite informa¬ 
tion can be obtained. He looks very ill, and his face is drawn 
and pinched, but otherwise expressionless. 

Mental state .—Patient is confused, very self-satisfied, his state¬ 
ments appear to be altogether unreliable ; he occasionally replies to 
questions, does as he is told, or notices what goes on around him. 
He says he is married and that his age is 29. He has “ a lovely 
wife and a beautiful daughter, he has been married sixteen years, 
he has nineteen daughters, he can work the typewriter and is a 



printer, he was a sailor and in the Navy.” When left to him¬ 
self he rambles on about going to Australia, to diamond mines and 
rambling about the coast. 

The discs are normal. They are both very pale and suggest 
moderate atrophy at first sight. Patient can, however, read easily 
with either eye at about the normal distance, and, consequently, 
the pallor is normal. 

October 10.—The patient’s mind is somewhat clearer, and he 
gave me the following account of himself. He had, in 1884, a sore 
followed by secondary symptoms for which he was treated some 
months with mercury pills. He was aged 20 at the time. A few 
years later he became acquainted with a woman who had left her 
husband, and they had lived together as man and wife up till six 
months ago, when she deserted him, and to this he attributed his 
mental affection. The history he gave, however, suggested that 
she had been compelled to leave him on account of his habits and 
infirmity. His illness began three and a half years ago with pains 
in the legs, difficulty with the bladder and bowels, followed by 
ataxy and ocular paralysis. He went to King’s College Hospital 
and was admitted under Dr. Ferrier. Soon after this he seems to 
have had an apoplectiform seizure and was taken up by the police. 
He has had loss of sexual power for three years ; this was pre¬ 
ceded by satyriasis. The woman he lived with bore him no 

Physical condition .—Knee and triceps jerks absent, plantar and 
cremasteric reflexes also absent. Joint sensation in toes lost, not 
however in ankle. Joint sensation in fingers lost, ataxic gait, 
inability to touch nose with eyes shut, hypotonus to a right angle. 
No anaesthesia of the trunk or limbs detected and no analgesia. 
This is fairly reliable. He has very marked tremor of the bps and 
tongue, and the speech is very slurred. The smell is defective, as 
he is unable to recognise the strong odours of assafcetida, cloves, 
or peppermint. His taste is good, recognises quinine, sugar, and 
acids. Pupils remain the same as when last examined. He is 
able to walk, and he volunteers the remark that he was much 
worse in this respect at one time. 

Mental condition .—His knowledge of time and place and 
memory are fairly good, but he has exalted and grandiose ideas 
about obtaining watches and jewels, and making large sums of 
money by pawning them. The attendant states that he is better 
and has control over his sphincters. 

March 1.—Death—Autopsy refused. 



Case 51.— Ataxy of some years duration in a man aged 39. Onset 
of cerebral affection manifested by epileptiform seizures , mania , 
with grandiose delusions . Death eighteen months after onset of 
mental symptoms . Marked cerebral lesions characteristic of 
general paralysis , and marked spinal lesion characteristic 
of tabes dorsalis . 

R. 8., aged 39, was admitted to Cane Hill suffering with mania 
and grandiose delusions. The history was that he had suffered 
for eighteen months from locomotor ataxy, for which he had been 
a patient at the Croydon Hospital. The supposed cause of his 
mental affliction was worry and family troubles occasioned by his 
loss of occupation as a gardener. He had been married eleven 
years, and had a family of five children. No history of syphilis 
was obtainable, and there were no signs on the body. 

Physical condition .—Nutrition poor, muscles wasted; he has 
marked locomotor ataxy. The pupils small, equal, inactive to 
light, react to accommodation. Knee-jerks absent ; gait, walks 
with a wide base, and is somewhat unsteady. Speech markedly 

Mental state. —Conversation rambling, irrational, and in¬ 
coherent. Says his brothers are coming up to the Croydon 
Flower Show, that they will stay three months ; that he has four 
elephants and fifteen horses. 

After two or three months in the asylum his ataxy considerably 
improved. From time to time he had convulsive seizures, from 
which he recovered, but his mental condition became progressively 
worse, although sometimes after the fits had passed over, he 
would apparently be somewhat brighter. He died of exhaustion 
of general paralysis eighteen months after admission. (Abstract 
of notes by Dr. Donaldson.) 

Summary of post-mortem notes .—Membranes thickened, 
opalescent, and adherent to the brain cortex; excess of cerebro¬ 
spinal fluid, all the ventricles somewhat dilated and markedly 
granular. Left hemisphere weighed 20 grammes less than the 

Summary of results of microscopical examination ; Brain .— 
Portions of the prefrontal, Broca’s, and central convolutions 
examined by Nissl and Pal methods showed the characteristic 
changes of a fairly advanced case of general paralysis, viz., 
vascular engorgement, thickening of membranes, proliferation of 
glia cells, dilatation of perivascular lymphatics, with cellular 
proliferation. Disarrangement of Meynert’s columns owing to 



acute and chronic destructive changes in the cortical cells, 
especially of the molecular layer and the small and medium sized 
pyramids. Atrophy and partial disappearance of the tangential 
and supraradial fibres, which is most marked in the prefrontal and 
Broca’s convolutions. 

Spinal cord . —All regions examined, and showed a naked eye 
disappearance (with glia substitution) of the intramedullary 
projections of the root fibres in the lower cervical, dorsal, and 
lumbo-sacral regions. The endogenous systems of fibres were in 
this case but little affected. The cornu commissural tract possessed 
the normal wealth of fibres ; there may have been some sclerosis 
in the comma tracts in the mid-dorsal region, but there was an 
abundance of fibres in the posterior internal zone, and these could 
be traced to the lower dorsal region as a strip of fibres amid the 
sclerosed tissue extending along the periphery of the cord, and at 
a lower level massing into a small triangle* which, again, at a still 
lower level, could be followed as the septo-marginal ending in the 
oval area in the lower lumbar region, and finally continuous 
with the median sacral triangle. 

GROUP 4.—Tabo-paralysis with Marked Speech Affection. 

Case 52.— Tabo-paralysis , five years' duration from onset of 
symptoms , history of hereditary insanity in mother and brother. 
All the family in the publican line and given to drink. The 
disease commenced with fits , speech affection , alternate excite¬ 
ment and depression , grandiose and sexual delusions and 
perversions. Considerable ataxy without anesthesia , or loss of 
joint sensation. Superficial and deep reflexes exaggerated . 
Death from dysentery . Typical general paralytic brain , 

direct and crossed pyramidal degeneration of spinal cord and 
typical posterior column degeneration of ataxy. No degenera¬ 
tion of posterior roots or Lissauer's tract of fine fibres; only 
coarse fibres of entry going to cornu radicular zone . Cord 
very small. 

B. C. A., aged 50. Admitted to Colney Hatch, May 29, 1900. 
Occupation for fifteen years barman and cellarman, then barber for 
six years, and finally for the last seven years willing to take any odd 
job such as painting and decorating. From the account he gives 
me he evidently lived a very racketty life, drank hard and indulged 
in marked sexual excess. He denies venereal infection, but there 
is a scar on the right groin, enlarged inguinal glands, and several 
papery scars on the legs. He says he has three children, the first 
of whom was born five years after marriage; two twins had 



previously died. It was ascertained that his brother Walter had 
been in the asylum fifteen years, suffering with delusions of 
persecution, attempted suicide—cause drink and heredity. Mother 
died in asylum forty years ago, went out of her mind on 
account of worry brought on by her husband’s gambling, drinking, 
and immorality. For two months prior to admission to the asylum^ 
he had been having fits. This agrees with the statement of his 
wife in the Case Book. Prior to admission the wife states he was 
at times violent, at other times depressed. She and her children 
were afraid of him when he was violent. She said that he had 
similar fits some years before admission; he had recently become 
intemperate and given way to gambling. She had noticed an 
alteration in his speech two years before admission. 

Physical condition .—He has an ataxic walk, heels down first, 
wide base and considerable incoordination. He has no cord-like 
constriction, he has no difficulty with his water or bowels. Knee- 
jerks brisk on both sides, muscles well-developed and strength 
good. There is marked hypotonus of the hamstring muscles both 
sides and incoordination in the legs, thus he could not place right 
heel on his left foot or knee, with his eyes shut. No loss of sense 
of position of joints, and no anaesthesia of the skin could be detected, 
nor was there any delay in response. Superficial reflexes all 
markedly increased. Romberg’s symptom very slight. Speech 
very slurred and indistinct. According to the attendant it has 
become progressively worse. Tongue tremulous and very jerky 
on protrusion, marked tremor of the lips. Pupils pinpoint, right 
2 mm., left a shade less. Inactive to light, react to accommo¬ 
dation. Roughly tested colour vision normal, no limitation of the 
visual field. 

Mental condition .—He principally exhibits exaltation, delusions, 
and mild progressive dementia. Expression is rather vacant, but 
is easily excited to mirth especially when relating his love affairs 
and virility (sexual delusions and perversions). Orientation time 
and place fairly good. His memory he says was fairly good. 
He knew correctly that his wife came to see him last Sunday with 
his eldest son. He seems to give a rational account of his two 
sons’ employment. He gives correct answers when asked to 
multiply three by four and six by seven; still answers correctly 
when the figures are reversed. He remembers songs and words 
well. Mentally he is not much demented considering the very 
marked speech affection. He has had no fits since he has been in, 
there is more difficulty in articulation than anything else. He 
reiterates that too many women is the cause of his illness. He 



thinks that if he puts camomile poultices over himself, he would 
be quite well. 

Death on January 28 of aeute dysentery. 

The brain showed very marked wasting of fronto-central 
regions, thickening of all the membranes and atrophy of the con¬ 
volutions everywhere to some degree, but especially in the frontal 

and central re¬ 
gions. Cortex 
diminished, stri- 
ation very indis¬ 
tinct. Ventricles 
dilated, epen¬ 
dyma granular. 
Naked eye ap¬ 
pearances typi¬ 
cal of general 
paralysis. There 
was a naked eye • 
change in the 
posterior and 
to a less degree 
in the lateral 
columns of the 
spinal cord 
which could be 
fairly accurately 
localised after 
hardening in 
Muller’s fluid. 
The degenera¬ 
tive atrophy oc¬ 
cupied the root 
Fig. 36 . zone ; through¬ 

out the cord it could be seen distinctly 
entering Clarke’s column, and in the upper 
dorsal and cervical regions there was 
obvious degeneration of Goll’s column. 
Further particulars are given in the com¬ 
plete microscopic examination. 

Spinal cord .—The diagram indicates the 
degeneration which could be seen after a 
fortnight’s hardening in Muller’s fluid. It 
does not represent the actual degenera- 


tion which was found by Marchi method, which I will now 
briefly describe. 

Lowest cervical and upper dorsal. —Recent degeneration in 
crossed and direct pyramidal tracts, degeneration in root zone, 
some slight degeneration in comma tract. 

Mid dorsal .—Very marked degeneration in root zone, in cornu 
radicular zone, both crossed pyramidal tracts and comma tracts. 
The same applies to the lower dorsal. At the base of Clarke’s 
column are seen a number of fine degenerated fibres (collaterals), 
proceeding from situation of crossed pyramidal tract. 

Litmbo-sacral. —Marked degeneration in cornu radicular zone, 
root zone, septo-marginal and oval area, very numerous fine black 
particles in the pyramidal tracts of both sides, and a few, but not 
nearly so many coarse fibres as in the sections above described. 
In the attached roots of not one of these segments examined (and 
a large number of sections were looked through) could I observe 
any degenerated fibres in the posterior roots by the Marchi 

Conclusions. —It appeared, therefore, in this case at any rate, 
that the degeneration commenced in the intramedullary portions of 
the neuron. Many sections showed an attachment of the nerve 
roots entering the cord (vide photomicrograph, fig. 41, p. 274). No 
degeneration extramedullary, but immediately after piercing the 
membranes (and therefore losing their primitive sheath), the fibres 
are completely degenerated. 

This acute degenerative process is very interesting as showing 
either support for Redlich and Obersteiner’s Theory of Meningeal 
constriction, or, as I believe, an acute primary degenerative pro¬ 
cess commencing in the portion of the neuron where the primitive 
sheath is absent. The membranes are not thickened over the 
posterior columns nor at the root entry. Another point of interest 
is that although there was a considerable outfall of exogenous 
fibres in the lumbar enlargement as shown by the Weigert method 
of staining, yet a considerable number of fibres can be seen entering 
the root zone. Of course, a great number of these may be 
degenerated as shown by the Marchi method. 

Such an amount of degeneration would, I think, under ordinary 
circumstances, have been sufficient to abolish the knee-jerks, but 
there was a crossed pyramidal degeneration both Bides. There 
was very considerable recent degeneration of descending and 
ascending endogenous fibres, and this may partially account for 
the pronounced ataxy. 



Case 53.— Tabo-paralysis , first symptom inability to use his tools , 
then has left-sided fits , affection of memory and speech , de- 
velopment of ataxia , wo cutaneous se?isory or visceral symp¬ 
toms. The degeneration apparently has affected the motor 
afferent and efferent systems , and the kincesthetic centres of 
verbal and written speech. No delusions. 

J. F., aged 36, cabinet-maker, transferred from St. Pancras 
Workhouse Infirmary to Hanwell, December, 1901. In April, 
1899, he was an outpatient at Queen Square Hospital under 
Dr. Beevor, who has kindly furnished me with the following 
notes :—Syphilis ten years before. History of two fits left-sided. 
Pupils R. > L. reacted to accommodation, not to light. Tremor 
in tongue and lips. Speech suggested general paralysis. Men¬ 
tation slow, fixation bad. Romberg’s symptom, ataxic gait. 
No lightning pains, no anaesthesia, no analgesia. Sphincters not 
affected. Memory very bad, nil ophthalmoscopic. Diagnosis 
general paralysis or tabes, with an inclination to the former. 

This account closely corresponded with the account the patient 
gave me concerning the fits and his subjective symptoms, so that 
his answers may be considered reliable as to his present condition. 
Married seven years, no children and no miscarriages. There is 
a scar in the groin, cervical and inguinal glands enlarged. He 
states that he was treated with strychnine by Dr. Beevor, and 
that he had had two left-sided hemiplegic attacks affecting his 
speech and memory. He fell down suddenly in the Euston Road, 
losing his senses, and when he came to, his speech was affected 
and his memory bad. He states that for some time previous to 
the fits he was unable to do his work, because he could not use 
his tools. 

Physical condition. —His gait is markedly ataxic. Romberg’s 
symptom marked. He has no pains. There is incoordination in 
the hands and some loss of sense of position. He suffered with 
bladder trouble while in the workhouse, necessitating use of 
catheter. He has now no control over the sphincters. Never 
had double vision. Pupils 4 mm., irregular, A. R. Knee-jerks 
absent both sides, triceps and wrist tap obtained on both sides. 
Some incoordination in the hands. Face congested, flushed, greasy 
skin, emotionless, blank expression. Tongue and lips tremulous, 
speech hesitant and syllabic. Sensory. No analgesia or anaes¬ 
thesia discovered anywhere. Superficial reflexes present. 

Mental state. —Slow reaction. Thinks he is in St. Pancras 
Workhouse, he knows the day of the month, but there is a 


moderate amount of dementia. He has no delusions, halluci¬ 
nations, or illusions. 

April 9, 1902.—Physical condition very much the same, 
except that he is more helpless. He lies with legs and thighs 
semi-flexed, but feet plantar flexed and inverted owing to weak¬ 
ness of dorsal flexors of feet and peronei. The feet are blue and 
cold, and the plantar reflexes are now absent. Epigastrics are 
present. It is impossible, owing to his mental state, to test in a 
reliable manner his cutaneous sensibility; but there is undoubtedly 
hypalgesia all over the body, and analgesia of the lower part of 
trunk and legs. There is paresis of left external rectus and 
double vision. Pupils 4 mm., equal A. E. He cannot stand 
without support, and if he closes his eyes he sways to and fro. 
His speech is very syllabic and slurred. When asked to write he 
was unable ; he tried to hold the pencil between the middle and 
ring fingers, closing his fist, but he could make no movements, 
and dropped it. He cannot walk without assistance; the gait, 
when supported by an attendant, was noted. He walks with 
rather a wide base, brings his heels down first, throws out and 
circumducts advancing leg so as to clear the ground with the 
foot which is plantar flexed and inverted ; he does not flex the 
knee at the commencement of the step, but keeps it extended, 
and the ground is cleared by abduction and circumduction of 
the leg. He uses his right leg more than his left for progression. 

Case 54.— Tabic paralysis, Babinski’s sign, successive right-sided 
fits, absent knee-jerks, aphasia, hemiparesis and hemianesthesia 
of a temporary character at first, but followed later by per¬ 
manent defect, death in a fit, great wasting of left hemisphere, 
no coarse lesion, marked pyramided degeneration, direct and 
crossed in the cord, with old posterior column sclerosis. Large 
amount of cholin in the blood. 

D. G. W., aged 45, journalist. Was admitted into Charing 
Cross Hospital, February 20, 1902, having fallen down in a fit. 
The next day when I saw him he was conscious, but unable to 
speak or write, nor did he seem to understand what was said to 
him. When talking to the students on his case, he behaved like a 
man who was listening to a foreign language, and who understood 
every now and then a word that was said. The pupils are 
unequal and inactive to light, active to accommodation. The 
knee-jerks are absent on both sides, and there are typical 
syphilitic scars on the legs. The plantar reflex on the right side 


gives a well marked extensor response ; there is some rigidity in 
both the right arm and leg, and hemiparesis. Slight paresis in 
the lower part of the face on the right side; lips tremulous, 
tongue tremulous, protruded very slightly to the right. Diagnosis 
tabic-paralysis. A few days later I ascertained from a relative 
that this patient had been treated for locomotor ataxy. He also 
informed me that the patient had for some time acted strangely. 
There was no history of insanity in the family. The patient in a 
few days partially recovered his speech. He left the hospital, had 
another fit, and was taken into King’s College Hospital; there he 
became troublesome, showed signs of dementia, and was Certified 
and transferred to Claybury Private Asylum, March 11, 1902, 
where I saw him again. He did not recognise me, although he 
was able to speak now, and to tell me that he was a journalist 
connected with the Globe newspaper. I made the following notes : 
There is no doubt that he is suffering from paralytic dementia with 
tabetic symptoms. His speech is hesitating, stumbling, and words 
are occasionally clipped and slurred; his comprehension is poor, 
and he has marked loss of memory, in consequence of which he is 
incoherent and rambling in his conversation. His orientation is 
defective. Pupils unequal, irregular, left the larger, both react 
very sluggishly to light. March 22, the patient gradually became 
hemiparetic on the right side; the arm showed entire loss of 
muscular sense and tactile sensibility, though general sensibility 
from the coarse point of view was present; he was unable to 
perform any voluntary movement with it, but simply made 
spasmodic attempts to do what was desired; he could not place a 
pencil in the hand owing to the extreme anaesthesia of the fingers. 
The grasp, however, in the right hand was very good on bilateral 
squeezing, although delayed, and he was also able to perform 
bilateral movements, such as raising both arms above the head, 
and putting them in various positions, especially if the action was 
first performed once or twice by the left hand. He occasionally 
got a word out, but very rarely, most of his replies being of the 
nature of gibberish. He, however, understood perfectly all that 
was said to him, and at times, when not endeavouring to use 
a particular phrase or word, got out a short reply quite distinctly. 
Eight lower face paretic. These facts, together with subsidiary 
details not referred to, point almost conclusively to a temporary 
cortical vascular disorder, involving in order of severity the face, 
arm, and leg areas. 

At the commencement of April he began to get wet occasionally, 
and more demented. Since the last fit he has not recovered the 


power in his right arm. The mental condition became worse, and 
on. June 13 he had another fit, became unconscious, and died 
suddenly in a convulsion, 3.25 a.m. 

Abstract of post-mortem notes .—Cause of death, exhaustion, 
general paralysis. Cerebral hemispheres, right 542 grammes, left 
480 grammes. Ventricles.—Dilated and granular, especially the 
fourth. Pia-arachnoid.—Thickened and somewhat opaque, espe¬ 
cially over frontal and central regions of left hemisphere, which is 
markedly atrophied. Spinal cord.—After hardening in Muller for 
two days, exhibited characteristic gray degeneration of posterior 
columns, degeneration of both crossed pyramidal tracts and the 
direct tract of the left side, very obvious to the naked eye. The 
blood taken from this case yielded, comparatively speaking, a large 
amount of choline, thirty minims of blood being sufficient to show 
large numbers of octahedral crystals of good size of the double 
salt of choline and platinum. All the vital organs were, to the 
naked eye, perfectly healthy; there was no obvious organic 
disease; the body was well nourished, and no morbid appearances 
presented themselves, except in the above-mentioned cerebral 

We might, therefore, presume that the patient may have really 
died from toxaemia ; for although choline is a comparatively 
feeble poison, yet with other bodies of the cholin group existing 
in the blood and cerebro-spinal fluid in such large amount as the 
above test indicates, might suffice to produce toxic effects. 

Naked eye examination of brain after hardening in Formol - 
Muller and stripping the membranes .—On both sides there is 
thickening of the membranes, the left hemisphere is obviously 
smaller than the right, the convolutional patterns of the two 
hemispheres are complex, and pretty closely resemble one 
another in the form, number and distribution of the sulci and 
convolutions. Placed with the mesial surfaces in apposition, 
the top of the fissure of Rolando on the two sides being made 
to approximate, it is shown that the prefrontal tips also approxi¬ 
mate, and there is convolutional symmetry in size, and fairly 
in form of the halves of the cerebrum; but behind the fissure, 
all the convolutions of the left hemisphere are markedly 
atrophied, especially the ascending parietal, the para-central 
lobule, the angular and supramarginal convolutions, so that the 
tip of the occipital lobe of the right hemisphere projects quite half 
an inch further back than the left—this being mainly due to 
atrophy of the convolutions behind the fissure of Rolando. The 
temporal lobe of the left hemisphere is smaller than that of the 



right, and especially noticeable is the difference in size of the first 
temporal on the left as compared with the right side. The 
posterior third of this convolution is very small and atrophied. 
The atrophic process then has affeoted, especially in this journalist, 
the auditory and visual word centres. The appearances of the 
left half of his brain conforms to the symptoms manifested during 
life, viz.—sensory aphasia and paraphasia, confused ideation of 
verbal and written speech, although he could utter articulate 
sounds. His speech defect was not like that of an ordinary 
general paralytic. Preliminary microscopical examination of 
the brain showed characteristic changes of an acute nature, 
cell and fibre destruction, glia proliferation, plasma cells around 
the vessels. Medulla and spinal cord.—Abundant degenera¬ 
tion was found by the Marchi method in both pyramids of the 
medulla, especially the left, and in the left direct and right 
crossed pyramidal tracts (vide fig. 42). There were also numerous 
degenerated fibres in the right direct and left crossed pyramidal 
tracts. By the Weigert method there was naked eye degenera¬ 
tion of the left direct tract in the cervical region, and of the 
right crossed pyramidal tract, and to a much less degree the 
left throughout the cord. The crossed pyramidal and pre- 
pyramidal tracts on both sides stain indifferently as compared 
with the rest of the antero-lateral regions of the cord, as if there 
was some chemical change in the myelin apart from the sclerosis 
due to overgrowth of glia tissue. The posterior columns show a 
marked sclerosis corresponding to the disappearance of the intra- 
spinal projections of the posterior roots. There ip a naked- 
eye sclerosis of' Goll’s column in the cervical region; marked 
atrophy of the cerebello-petal fibres of the lumbo-sacral roots, and 
correspondingly of the plexus of fibres around the cells of Clarke’s 
column in the lower dorsal and upper lumbar segments; and 
marked atrophy of the root zone in the lumbar and sacral regions. 
The lower lumbar and sacral roots are considerably denuded 
of fibres, half to one-third. Lissauer’s tract of fine fibres is 
apparently little or not at all affected. There is no atrophy of the 
endogenous systems of fibres. The septo-marginal and oval area 
and sacral triangle show no outfall of fibres. The symptoms and 
signs observed during life can be explained by the morphological 
changes. The spinal lesions correspond to an early condition of 
the first stage of ataxy in which the skin sensibility of the soles 
persists, hence the plantar reflexes were obtainable. On the 
right side there was marked sclerosis of the crossed pyramidal 
tract, hence the extensor response in the sole reflex. Although 



there was this marked pyramidal degeneration, the knee-jerk did 
not return, because of the extensive degeneration in the root zone 
breaking completely the reflex path of spinal muscular tonus. 

Case 65.— Tabetic general paralysis , in which noticeable symptoms 

were first mental, and subsequently spinal. No history of 

insanity in the family. Analgesia all over the body. 

H. E., aged 38, admitted to Hanwell, January 29,1896, occupa¬ 
tion carman, married and children, always been a total abstainer, 
no family history of insanity, fits, phthisis, or nervous disease. 
There is a large scar on the penis, admits having had syphilis and 
having been treated for it. He has enlarged glands in the groins. 
His illness commenced in 1895. He became irritable, falling into 
heedless passions, would get up at night and run out of doors, 
threatening his wife and children with violence. He then began 
to stagger in his walk, his speech became indistinct, and his 
memory weak. 

History (obtained from wife, June, 1900).—H. E., now aged 42, 
occupation carman, married at 23, seven children resulted from 
marriage, five of whom are alive, and two dead, aged 11 months 
and 14 months respectively. Wife had one miscarriage. Six 
months before he went to Hanwell patient became very irritable 
and forgetful, nothing pleased him. He complained also of giving 
way of his legs, and of pains, which he thought were rheumatic, 
in his arms and legs. Pains were shooting in character. He 
complained also of pains in the stomach, with appearance of a 
lump that disappeared. Wife noticed that he had a difficulty 
with, and that there was a hesitancy in, his speech. Patient was 
a very temperate man. There is no history of insanity in the 
family on either side. Before his illness patient was a good 
husband and father, a strong man, of a very-easy-going placid dis¬ 
position, and bad nothing to worry about. He used to sleep well. 
She brought her boy to the hospital to see me, as she feared he 
might be going like his father; the following notes were made:— 

A. E., aged 13 years, the fourth child of the marriage. When 
he left school he was in the fourth standard. He was discharged 
from the Farm ■ School for having stabbed two boys; he knew 
perfectly well what he was doing. Knee-jerks weak, only obtained 
by reinforcement, pupils equal, react to light and accommodation, 
no tremor in speech. The boy’s mother notices no difference in 
him, he is good and affectionate. He suffers with headache now 
at times, affecting the back of the head, but he is never sick. His 
knowledge of time and place is good, simple judgment also good. 



He laughs and talks in his sleep, and does not rest properly, but 
he never wets the bed. No history of fits. He has lately had a 
discharge from the ear ; glands are a little enlarged. 

September 26, 1900.—The following notes were made by me : 
About a year ago the patient had a congestive attack and remained 
in a dazed semi-conscious state for some days. He has had 
none since. He is childish, but has no marked delusions; his 
memory is poor, and his knowledge of time and place imperfect, 
but not absolutely lost. The speech is syllabic, hesitant, and 
slurred, tongue tremulous, and he has a mask-like expression 
denoting an emotionless state of the brain, but he occasionally 
bursts out into a childish laugh. He has an ataxic walk, the knee- 
jerks are absent, pupils medium sized, unequal, inactive to light, 
react to accommodation, complains of no girdle sensation, Romberg 
symptom well marked, considerable degree of hypotonus of 
muscles of the legs, the legs being capable of being bent at the hip 
to a right angle. He nowhere feels the prick of a pin, not even in 
the meatus urethras, but responds with some delay to touch all 
over the body. When you prick him he says that it is a touch. 

June 18,1901.—Some time ago the patient commenced to have 
fits affecting the right side, followed by loss of use of the right 
limb, and the speech became even more indistinct and slurred. 
The hemiplegic condition has somewhat improved, but one can 
still see continuous involuntary twitchings in the right leg. Lying 
on his back he can voluntarily raise the leg from the bed, and he 
can use his arms without any marked incoordination of movement. 
The muscles are all very much wasted, and their power enfeebled, 
but the reason why he is unable to stand is mainly due to the 
ataxy. There is very marked hypotonus in both legs, and the 
deep reflexes are lost. He has no power over the bladder, and 
the water dribbles away continuously into the bed. Although the 
speech is so markedly affected, the dementia is rather childishness 
than anything else. He takes an interest in his surroundings, 
and an elementary knowledge of time and place is not wanting. 
He told me spontaneously that his neighbour had been in the 
asylum eighteen months, which was correct. 

. August 20.—A fortnight ago the patient had an attack of 
vomiting, very severe, which lasted for two days, accompanied 
with diarrhoea. He has not spoken since then. He is quite 
helpless, lying in bed on his back, did not recognise me, but he 
recognised Dr. Spark, and apparently made an attempt to speak. 
He is very emaciated, has complete loss of control over the 
sphincters, epigastric reflexes just present left side, absent right, 


plantar reflexes present both sides. Pupils, right, 6 pam., left 
5 mm. 

The patient died September 10, 1901, of dysentery, of which he 
had suffered several attacks. The whole large intestine was in a 
state of acute and chronic ulceration. The brain, spinal cord, 
nerves, and muscles were removed by Dr. Bolton, and, owing to 
the softness of the central nervous system, the two former were 
placed directly into formaline, in order that they might be har¬ 
dened before any descriptive examination was made. • After a 
fortnight in this solution the brain and spinal cord were examined. 
The hemispheres show but little thickening of the pia-arachnoid 
generally, and there was not much "wasting. Each hemisphere 
weighed 633 grammes ; the cerebellum and pons, with the 
medulla, 140. There is some thickening of the pia : arachnoid 
over the mesial surface of both frontal lobes, especially the left. 
There is also tbuekening of the membranes oyer the left hemi¬ 
sphere in the following regions : the lower part of the Bolandic 
area, the adjacent Broca convolution, and the anterior portion of 
the first temporal. There is wasting of these structures, as is 
shown by the fact that the anterior portion of the Sylvian fissure 
is wider on the left than on the right side. It is covered, more¬ 
over, with thickened pia-arachnoid membrane. The bases of the 
first and second frontal convolutions and the adjacent portion of 
the ascending frontal are obviously wasted as compared with the 
right. The intervening sulci are deeper and the covering pia- 
arachnoid thicker and more opaque. The lateral ventricles are 
apparently not much dilated, but the ependyma is slightly 
granular, likewise the ependyma of the fourth ventricle. The 
spinal cord appears smaller than natural, but does not look 
flattened posteriorly. The posterior roots in the dorsal and 
lumbo-sacral regions, especially the latter, appear smaller and 
more gray and translucent than normal. On cutting the cord 
transversely, obvious naked-eye degeneration is visible in the 
posterior columns, exhibited by gray-red translueency as com¬ 
pared with the dead white of the antero-lateral columns, 

Case 56.— Tabo-paralysis of motor type , which commenced with 
occasional attacks of transitory loss of speech ; History of 
insanity in family . Grandiose delusions and alteration in 
manner and disposition . Admission to asylum , on, account 
of acute maniacal symptoms , development of motor paresis and 
ataxy; subsidence of mental symptoms , very little dementia. 

A. A., admitted to Hanwell, May 4, 1901, aged 40. Occupa¬ 
tion, for a long time manager of Sanger’s Circus. Has travelled 



all over the world. Latterly, since he has lost his place, which 
has worried him a great deal, he has been a string bag maker. 
He has been married eleven years, no children, no miscarriages, 
steady and temperate. Father and paternal grandfather were 

History of present illness (from wife).—Two years ago he 
suffered with occasional attacks of transitory loss of speech and a 
bewildered look. Two or three months ago he became altered in 
manner and disposition, turned against his wife; and imagining 
he possessed thousands of pounds, indulged his extravagant ideas 
by buying useless articles. 

Physical condition .—June 28,1901. Walks with a wide rather 
ataxic gait, knee-jerks not obtained, some unsteadiness with the 
eyes shut, expression rather emotionless, tremor of tongue and 
face muscles, marked slurring and hesitancy in speech, pupils un¬ 
equal, right 6 mm., left 5 mm., inactive to light, active to accommo¬ 
dation. Well marked syphilitic history, parchment scars on the 
body. There is a suppurating corn on the right little toe, now 
healed; marked hypotonus of hamstring muscles, no loss of joint 
sensation, no analgesia. 

Mental condition .—He shovte very little mental defect, he is 
able to give a rational account of himself and his doings in the 
past. He haB no grandiose delusions now, and his knowledge of 
time and place are only slightly defective. There is no incoher¬ 
ence in his conversation, in fact, his disease appears to have 
affected especially the motor tracts. 

July 4, 1901.—Pupils the same, mental and physical state 
unchanged. No outaneOus anaesthesia of thorax. 

October 4.—Simple-minded, officious, declares that he feels 
quite happy. He has a perforating ulcer on the right foot, which 
causes him a lot of trouble at times. 

October 30.—Perforating ulcer of right ball of little toe, also 
com over ball of great toe. Speech much affected. No loss Of 
joint sensation, no analgesia of feet and legs, no thoracio 
anaesthesia. Pupils equal, right slightly irregular, no reaction to 
light, slight reaction to accommodation. No attacks of sickness, 
no bladder trouble, Eomberg symptom slight. Twenty years ago 
he had syphilis; there is a scar of an old gumma on the right 
thigh. Deep reflexes of legs lost. Mentally he is only slightly 
exalted; the facial expression also denotes exaltation of only a 
slight degree. He is clean in his habits. 

June 19, 1902.—Suppurating corn on right little toe. He has 
no loss of joint sensation and no analgesia. 



April 9, 1902 .—Physical condition .—He walks with a slightly 
ataxic gait, the feet apart and bringing the heels down first. 
Knee-jerks absent both sides even with reinforcement. Lying in 
bed on his back, weakness of dorsal flexors of both feet noticeable 
in synergic actions of flexion of hip joints. Bypotonus of hamstrings 
equal on the two sides. Slight loss of sense of position in feet. 
None in hands. No loss of joint sensibility detected in feet or 
hands. No cutaneous anaesthesia or analgesia. No shooting 
pains in legs, no girdle sensation, no bladder trouble. All super¬ 
ficial reflexes present, also deep reflexes in arms. SwayB a little 
with eyes shut, but can stand, though with some difficulty, on one 
foot. Speech is markedly affected, tongue and face muscles 
tremulous. Yaso-motor-paresis of vessels of face. He has lately 
had a number of congestive and epileptiform seizures. 

Mental condition .—He is not the subject of delusions or hallu¬ 
cinations and he is only slightly demented as he can converse 
On most subjects rationally and his memory is good. He told 
me that when he reads it is not necessary for him to read the 
words silently ; he can do it by visual impression only. 

Case 57 .—Tabes following injury, modified gastric crises, causing 
delusions that his stomach had been swollen to enormous size. 
Death from tabo-paralysis. 

L. H., aged 35. Admitted February 16, 1902, died May 31, 
1902. Dock labourer, married. 

Dr. Jones' note (February 21st, 1901, Claybury Asylum).— 
He is suffering from tabetic paralytic dementia. Mental reaction 
slow, and he has impaired memory, loss of knowledge as to time 
and place. He is somewhat depressed, and cannot realise where 
he is. He does not think there is anything the matter. He tells 
me he has six children, but he shows no concern to get to them 
and look after them. There is marked dementia. He is in fair 
nutrition, health impaired. Eight pupil reacts slightly to light, the 
left less; both are irregular, the right*rather smaller. Knee-jerks 
absent. Common sensation in the legs retarded, cannot tell 
quickly when pin-pricked. Cannot stand blindfolded, and there 
is a tabetic gait. 

January 9, 1902.—Mental reaction slow, is entirely lost to 
his surroundings, expresses delusions freely, says he is being 
worked on by electricity. He is fairly well nourished, has 
symptoms of tabes dorsalis. Knee-jerks absent, pupils react 
sluggishly, marked incoordination. Very fine facial tremors. 
Eomberg’s symptom. 



History (from wife).—Dock labourer. Married twelve years. 
Four children alive, two dead, the first and last, eldest living 11 
years, youngest 3£ years. Sister suffers with epilepsy. Seven years 
ago he had an accident, a bag of sugar weighing 2£ cwt. fell across 
the back of his neck. He was in London Hospital two days. 
Unable to work for three months, and received £15 compensation 
from his employers. Three years after the accident he commenced 
to have rheumatic pains, and pains in the stomach which were 
thought to be dyspepsia at the London Hospital. Complained of 
his head, and was very irritable. Always a man of moods ever 
since she knew him. He has experienced difficulty with his 
water and bowels, being very costive. He would go without food 
for days because of pains, but was not sick. He always said he 
felt as if something was drawing him in. Complained of crawl¬ 
ing sensations. He had a kind of fit eighteen months ago when 
he was taken into sick asylum, then he tried to get out of the 
window. Transferred to Poplar, and then here. He was a good 
husband and a good father. Frequently visited by wife, who 
noticed that his mind became weaker each time. .He had no 
fits that she knew of. Always complained of the pains and the 
dyspepsia, even recently when she visited him. Very much 
wasted. Syphilis doubtful. (F. W. M.) 

Medical certificate .—He is under the delusion thak his 
stomach has been swollen to an enormous size, also that people 
have conspired to put him away. At times he is quite lost in his 

Communicated by wife .—Strange in his manner, rambles in 
his statements. He was under the delusion that his body 
became swollen and of an enormous size. 

Post-mortem notes .—State of nutrition and muscular system 
emaciated. Syphilis, no visible scar on penis; history of one 
in private nojes made by Dr. Bolton, Skull somewhat dense. 
Average frontal thickness 6 mm., parietal thickness 3£ mm., 
occipital thickness 7. mm. • Pupils equal. Subdural space.—- 
Marked excess of fluid. Pia.—A little fronto-parietal milkiness, 
marked prefrontal adhesions and tearing of cortex on separating 
prefrontal lobes. Encephalon.—1,340 grammes, exceedingly 
cedematous. Weight of right hemisphere, 565 grammes ; weight 
of left hemisphere, 550 grammes. General wasting of convolu¬ 
tions, obscured by oedema. Ventricles immensely dilated and 
granular. Cerebellum weight, 170 grammes, oedematous. Fourth 
ventricle. — Markedly granular, especially calamus. Cranial 
nerves.—(Edematous. Spinal cord as small as that of a child of 



two years in the dorsal and lumbo-sacral regions. Obvious gfay 
atrophy of posterior column, but no flattening of the posterior 
surface, soft meninges opaque and thickened. Thorax.—Bronchi 
a little congested. Bronchial glands oedematous. Bight lung, 
weight 535 grammes, congested and broncho-pneumonic. Left 
lung, 415 grammes, more congested and broncho-pneumonic than 
right. Heart—A little wasted, weight 205 grammes. Aorta 
and great vessels.—A small amount of early atheroma. Abdo¬ 
men.—Liver weight, 1,150 grammes, muoh congested, density 
increased. Spleen, weight 78 grammes, density much increased. 
Bight kidney, weight 95 grammes, cortex 4-5 mm., density in¬ 
creased ; strips fairly readily. Left kidney, ditto. Abdominal 
aorta.—Slight early atheroma. Stomach.—Patchy congestion 
and chronic catarrh, also fibrosis. Small intestine.—Chronic 
catarrh and patchy congestion. Large intestine.—Considerable 
patchy congestion and catarrh. Abdomen.—Immensely dis¬ 

Cause of death. —Broncho-pneumonia and bed-sores. General 

Microscopical examination of the brain (by Nissl method).— 
Ascending frontal and parietal, and parietal lobule.—Acute and 
chronic cellular changes, glia cell proliferation, increased vascu¬ 
larity,, the perivascular lymphatic sheaths distended and filled 
with plasma cells, also a number of lymphocytes. The vessels 
in the same instances are quite empty and collapsed, but pig¬ 
ment granules of altered blood corpuscles can be seen both free, 
and in the proliferated cells of the sheath. Many of the medium 
and larger sized pyramids show changes resembling acute experi¬ 
mental anaemia produced by ligation of tbe cerebral arteries. 
The cytoplasm and nucleus are swollen, the latter is clearer than 
normal, eccentrically situated and surrounded by crumbling cyto¬ 
plasm stained uniformly by fine dust like chromophilous particles. 
The processes of the cells are broken off and the cells are placed 
at all angles instead of in definite columns with their apical 
processes towards the surface. The small pyramids are similarly 
affected ; only as a rule more cells have entirely disappeared. 
The intensity of the destruction -varies in different situations 
in the same section. The cells of the molecular layer 
have entirely disappeared and there are numerous spider cells. 
There is cell proliferation, vascularity and thickening of the 
membranes. Some few of the Betz cells in the ascending 
frontal show marked chromolytic and nuclear changes. Some 
few are completely disintegrated, only a mass of very fine 



granular cytoplasm remaining with crumbled edges. Besides the 
above portion of the cortex, the first and second frontal, 
Broca’s convolution, central convolutions, posterior part of first 
temporal, angular and calcarine convolutions were examined. 
These all showed some of the changes described above, but the 
degree of severity of meningeal, vascular and cellular change is 
in the order mentioned, the changes in the occipital being very 
slight, for there is no meningeal thickening, and little or no 
abnormal vascularity, perivascular lymphatic dilatation or cell 
proliferation and but little dislocation of Meynert’s columns. 
Some cells show chromolytic changes, but the acute changes 
are much less obvious than in the fronto-central convolutions. 
The changes noted above are in all respects like those met with 
in an ordinary fairly rapid case of general paresis. 

GROUP 6.—Optic Atrophy and Tabo-Paralysis. 

Case 58.— Tabes, optic atrophy. Herpes zoster twelfth dorsal, 
tremor of tongue and lips, speech affection. Paralytic 
dementia in a man aged 26, seven years after infection .— 
{October 7,1900, Charing Cross Hospital.) 

R. M., aged 26. Labourer, previously leather dresser. No 
other neuropathic history, except uncle died in St. Thomas’s 
Hospital of nervous disease. Married five years Christmas, three 
children alive, one dead, lived one month. Twelve months ago 
patient saw double, and since then has suffered with shooting 
pains in the head, arms and legs, and pain around back. Eight 
months ago, suffered with weakness in bladder, cannot hold his 
water. Six months ago had difficulty in walking, especially in 
the dark. Eight years ago, chancre which lasted three or four 
weeks. Treated with iodoform at the Lock Hospital. No 
knowledge of any secondary symptoms. (It might be said that 
this was not syphilis, but I have seen so many cases treated for 
soft sore which afterwards developed brain syphilis, that I 
consider every venereal sore should be carefully watched and, if 
necessary treated. Only recently, within three months of infec¬ 
tion, a case came to my out-patients’, with optic neuritis and 
headache, and other signs of cerebral syphilis. He had only 
been treated locally. The patient recovered completely when 
placed upon mercurial inunction treatment.) Patient can stand 
with eyes shut and heels together, but cannot stand on toes. 
Cannot stand on left foot, but can on right. Knee-jerks absent. 
Pupils A.R., left 5 mm., right 4| mm., and irregular in outline. 
Sexual desire lost four months ago, but was not excessive before 



that time. Tongue and lips tremulous ; depressed anxious expres¬ 
sion on face, and suffers with frontal headache. Articulation fairly 
good. Has shooting pains in the back of ear. Patient has not 
slept well, but has had no dreams. 

Physical examination .—Old soar on dorsum of penis; glands 
shotty in neck and groins. Strength of muscles good. Marked 
hypotonus, extended legs can be moved to a right angle with 
body. Plantar, cremasteric and epigastric reflexes present. No 
loss of sense of position of hand. Tactile sensation good. In 
left foot and lower part of leg some prickB are felt as touch, or 
give the sensation of contact with a cold body. Pins and needles 
or shooting pains in legs and arms. No muscular wasting. Slight 
loss of sense of position of lower limbs. Some slight thermo¬ 
anaesthesia in legs and both feet. Nearly blind in both eyes, but 
the left iB more affected than the right. Primary optic atrophy 
both sides. 

July S, 1901.—Still pains in legs ; quite blind. Expression 
emotionless. Marked tremor in upper lip and tongue, slight 
hesitaney in speech, but no slurring. Has no fits, but suffers 
with headache occasionally. Still complains of weakness of 
bladder. Gan stand with heels together, but cannot stand on 
one foot; no ataxia in walking. Pupils right 5 mm., left 4| mm., 
both irregular in outline and inactive to light and pain, but react 
to accommodation and on convergence. On outer peroneal sur¬ 
face of right leg there is a patch of light tactile anaesthesia, a few 
spots scattered about on feet and legs where he does not 
appreciate a prick from a touch. Scars of herpes discovered 
right side area of twelfth dorsal. Superficial reflexes rather 
exaggerated. No thermo-anaesthesia. There is little change in 
sensory condition since he was here before. Although blind, he 
imagines that he sees people walking in at the door, and tries to 
get out of the way for fear of colliding with them. “ He has got 
mixed in his speech for the past few weeks.” 

Case 59.— Ataxy, optic atrophy, loss of memory, melancholia, 
visual hallucinations, delusions about his food, death from 

W. B. H., age 45, single, draper’s assistant, born in London, 
apprenticed at 16. At age of 30 contracted syphilis. Chancre 
(hard), followed by sore throat and falling out of the hair. He 
was treated for three months, but the gums were never sore. 
November 18, 1896, noticed dimness of vision of right eye, then 



lost his sight in fourteen days. Previous to this he. had 
insomnia for a long time. A few weeks later the vision of the left 
eye grew dim, and gradually became worse, until now he is almost 
completely blind. There is gray atrophy of both discs. His 
memory has not been good for several years. Four or five months 
ago he began to get weak in his legs; he is able to stand, but 
reels. There is no loss or delay of sensation to be detected in the 
limbs. The plantar and abdominal reflexes are brisk. The knee- 
jerks are absent. There is no local muscular wasting. He is 
emaciating, but he does not refuse his food. He can get up 
himself. The pupils do not react to light, are small and irregular; 
they react when he is told to look towards his nose. He has 
difficulty in micturition, but this may be explained by the fact 
that he has a stricture. 

Mental condition ,—He has visual hallucinations, and is very 
depressed. Painted up women, perfumed, come to him at night 
and taunt him. His facial expression indicates mental depression ; 
the lines are partially obliterated. The tongue is a little tremulous, 
there is no facial tremor. His memory of past events is fairly 
good, of recent events not good. There is a little hesitation in 
speech, but no syllabic difficulty. He cannot remember simple 
sentences which he is asked to repeat, e.g., one has to repeat word 
for word “ The Irish artillery extinguished the conflagration,” 
although he has not much difficulty in saying the words. 

August 10, 1898.—He complains of shooting pains in the 
stomach and in the legs. He can localise sensation of touch and 
pain accurately. He knows when and how his great toe is bent. 
The knee-jerks are absent. The pupils are small, inactive to 
light, but react to accommodation. He has a delusion that he 
has never left Australia, and is still there, and he says that his 
sister has never been, to see him, but that perfumed women come 
in to see him and make indecent overtures to him. His speech is 
slightly affected, being hesitant and tremulous. He says that his 
taste is good. Can hear a watch at one foot. No affection of 
taste, although he always says that there is something wrong with 
his food. He recognised salt and water perfectly. 

Summary of notes of autopsy .~Dura mater adherent in front, 
pia-arachnoid is thickened generally, adherent slightly to the brain 
convolutions. There is some vascular effusion along the upper 
border of the hemisphere. Fourth ventricle is granular, there is 
general slight wasting of the cerebral gyri. The optic nerves are 
atrophied. Weight of brain 47£ ozs. Heart, left ventricle slightly 
dilated, first degree chronic mitral disease and atheroma of aorta. 



Microscopical examination (by Dr. Hamilton Wright) .^Central 
and Broca’s convolutions; pia-arachnoid is thickened and its 
vessels congested. Nissl’s method shows Meynert’s columns in a 
disordered state, and a marked atrophy of many cortical cells. 
The processes of the latter are €t corkscrew M and are devoid of 
chromopbilous granules. Glia cells are exceedingly numerous and 
there are many spider cells present. The vessels are congested. 
The whole appearance of the cortex is as usually seen in cases of 
early general paralysis. Tangential fibres in Broca’s convolution 
and the part corresponding to it on the right side are wasted. 

Spinal cord .—Lower cervical region.—About one half of the 
fibres have disappeared from the posterior half of the postero¬ 
median columns. Many of these in situ are in a state of chronic 
wasting. There is marked atrophy of fibres along the anterior 
half of each intermediate septum. This atrophy passes backward, 
at the same time decreasing in amount, into the inner aspect of 
the base of each postero-external column. There is a slight de¬ 
generation of fibres in the root zones. All these parts are the seat 
of a sclerosis proportionate to the fibre atrophy. The rest of the 
posterior columns are practically intact. The roots external to the 
cord contain only a small number of unsound fibres. The posterior 
spinal ganglion cells of this region are healthy looking. The fibres 
from their distal ends are not obviously wasted. Thoracic region 
—The fibre atrophy and consequent sclerosis have practically the 
same distribution here as in.the cervical region. From the middle 
of the postero-median columns it tends to spread laterally into 
the median parts of the postero external columns. There is a 
slight degree of fibre atrophy in both root zones and in the roots 
external to the cord. The posterior spinal ganglion cells are not 
obviously wasted. The most marked feature is shrinking, probably 
artificial in origin. Lumbo-sacral region.—Wasting of proper fibres 
is marked along the postero-median septum in the upper lumbar 
levels ; also in the middle portions of the postero-external 
columns. In the lower segments the wasting has the same dis¬ 
tribution except that fibres in the position of the median oval area 
of Flechsig are almost intact. These pass backwards along the 
septum and tend to spread out along the periphery of the cord. 
The root zones are obviously wasted and sclerosed. Fibres in the 
position of the cornu-commissural zone are almost intact. There 
is a marked degeneration and denudation of root fibres external 
to the cord. Those still present are only in a few instances 
sound. Most are in some stage of chronic atrophy. Many cells 
of the posterior spinal ganglia in this region are in a state of fatty 



degeneration, and so give a purple reaction to Weigert-Pal hema¬ 
toxylin. The peripheral ends of the ganglia contain only a few 
wasted fibres in marked contrast to the proximal ends. 

It will be seen by the above that there is a moderate degree 
of wasting in, and a consequent sclerosis of, those parts of the 
posterior oolumns which contain exogenous or root-fibres. The 
endogenously derived tracts, i.e., the cornu commissural, descend¬ 
ing comma, Fleohsig’s median, and Gombault and Philippe’s tracts 
are practically healthy. The same may be said of the postero¬ 
internal zones. There is an intense congestion of all spinal, and 
spinal ganglion vessels. In the sclerosed areas these are slightly 

Case 60.— Optic atrophy, followed by tabes dorsalis, and later 
general paralysis. 

G. C., aged 36, porter, admitted May 27, 1894, to Marylebone 
Infirmary. Pour years before admission began to suffer with 
giddiness, bad sight, and squint. One year ago began to suffer 
with a staggering gait and also dropping things, for which he lost 
his situation. Rheumatic fever several times. Denies syphilis. 
Jaundice twenty years ago, and at that time was crushed in 
a crowd, which caused him to be laid up for some time with a 
pain across his back. Gait staggering, but Romberg’s symptom 
absent. He says he has difficulty in walking in the dark. Cutting 
pains in the legs, which are most severe in the left. Suffers with 
severe abdominal pains at times, probably gastric crises. 

Eyes.—External squint of left eye. Movements outward 
incomplete. No reaction to light or accommodation. White 
atrophy of both discs. Knee-jerks present, ankle clonus. Tender¬ 
ness over spine in the first dorsal, eighth dorsal, and lumbar 
region. Muscles good nutrition, no wasting. Sensation impaired 
all over face, chest, front, and both arms, with the exception of 
outer side of left arm ; sensations to cold also slightly impaired ; 
to heat, good. Leg sensation to touch almost absent, with the 
exception of the soles of the feet ; sensation to heat impaired. 
Both feet and hands are very cold. Bladder, at times cannot pass 
water. Colour vision very imperfect; pink he calls yellow, violet 
black, cannot pick out green and calls it drab, chooses yellow 
correctly; picks out mauve as being the nearest approach to 
red. Seen by Dr. Beevor on October 27. The case was diagnosed 
by him as one of posterior lateral sclerosis, with prominent 
hysterical element. “ The ankle clonus and generally increased 
reflexes were those of an organic lesion. The changes could only 



be of similar origin. The alterations of sensation were probably 
almost entirely hysterical. ,, Discharged December, 1898. For the 
above notes I am indebted to Dr. Lunn. Patient eventually died 
two years later at Claybury Asylum of general paralysis and 
septic meningitis. 

Case 61.— Optic atrophy , preataxic stage of tabes several years , 
attack of mania , grandiose delusions , epileptiform seizures , 
death , characteristic brain lesion, arrested cord lesion of tabes 
dorsalis , degeneration of crossed pyramidal tracts , heterotopia. 

J. W., age 37, agent, sent to me by Mr. Gunn from the 
Westminster Ophthalmic Hospital as a case of tabes in the pre¬ 
ataxic stage in 1893; attended my out-patient department, 
Charing Cross Hospital, for eighteen months. During that period 
there was little change in his condition. He presented the 
following symptoms: Failing sight, concentric limitation of the 
fields of vision, small pupils, unequal, A. R. No ataxy, Romberg’s 
sign not obtained. Shooting pain in legs, absent knee-jerks. 
Gutaneous sensibility was not noted. No signs of mental affec¬ 
tion. I lost sight of him, but eventually I remembered the 
name when I was taking his blood pressure some considerable 
time after his admission to Claybury Asylum in December, 
1896, suffering from mania and general paralysis. 

Family history (from brother, December 5, 1898).—Father 
intemperate; no consanguinity, no insanity. Patient has lived 
a very fast life with loose women, and has suffered with 
syphilis; latterly has had business worries, and six months ago 
he was very depressed and threatened to cut his throat. 

Physical condition. —Knee-jerks absent, walks with a shuffling 
gait, tremor of tongue and lips, speech slurred and syllabic, 
exalted expression. 

Mental condition. —Impaired memory, no idea of time or 
place, indifferent to his personal appearance and surroundings, 
delusions of wealth. * 

The dementia continued and progressed, and he had many 
epileptiform and congestive seizures, in one of which he died, 
May 14, 1899. 

Autopsy .—Nine hours after death. Body emaciated, left 
pupil 2 mm., right 3 mm. Legs are flexed at thighs and knees, 
there are large bed-sores over sacrum and great trochanters; he 
has numerous small, symmetrical, papery scars on both shins. 
The calvarium is thin, bloodless, frontal bone 4 mm., occipital 



6 mm. The pia-arachnoid was markedly thickened over frontal 
and parietal lobes, and slightly adherent to the cortex ; subdural 
space, moderate quantity of fluid. The basal vessels are the seat 
of a slight nodular arteritis. There is a slight wasting of first 
frontal and upper part of central convolutions on both sides. 
Cortical striae are fairly well marked. The white matter and 
basal ganglia are slightly cedematous ; no sign of softening or 
induration. The optic nerves on both sides are markedly atro¬ 
phied. Both lateral ventricles are slightly dilated, full of clear 
liquid, and moderately granular. The fourth ventricle is slightly 
dilated, but markedly granular. The spinal cord showed no 
naked eye change. Weight of right hemisphere, 563 grammes, 
left ditto. 

Lungs.—Bilateral septic broncho-pneumonia, which was the 
immediate cause of death. There is nothing further of note in 
the other organs. 

Microscopical notes (by Dr. Hamilton Wright).—Brain.—The 
posterior third of each third frontal gyrus was examined and 
found to be almost denuded of tangential fibres. Quite eight- 
tenths of them have disappeared. The cells are wasted and 
Meynert’s columns disarranged. The pia is thickened and its 
vessels congested. There is a large increase in the number of 
glia cells. The whole cortex is like that seen in cases of general 
paralysis of moderate duration. 

Spinal cord .—Cervical region.—The dorsal third of each 
postero-median column is slightly sclerosed. The sclerosis is most 
marked close to the median septum, and gradually diminishes in 
intensity as the intermediate septum is approached. The anterior 
third of these columns, except the apex, is also slightly scle¬ 
rosed. A few fibres seem to have wholly atrophied in these 
patches of scar tissue. The great majority of those in situ , are 
irregularly swollen or attenuated. The postero-external columns 
along the outer side of the intermediate septa are slightly 
sclerosed, and a small number of fibres have disappeared. The 
most anterior parts of these patches of scar tissue widen out just 
before reaching the posterior margin of the healthy cornu 
commissural zone. There is no sign of atrophy in the fibres of 
the postero-internal zones. Charcot’s root zones are intact in all 
segments of this region except the seventh and eighth. This is 
also the case in the extra-cordal portion of the posterior roots. 
In the seventh and eighth metameres there is a mild sclerosis 
and fibre atrophy in the root zones. A few fibres have disap¬ 
peared from Lissauer’s tracts. This, together with an atrophy of 



fibres in the same positions in the upper few thoracic segments, 
is enough to account for the sclerosis along the external margins 
of the intermediate septa in the higher cervical segments. In 
both crossed pyramidal tracts there is a moderate fibre atrophy 
and replacement sclerosis; the intermediate gray matter through 
which the motor fibres course is intact. This appears to indicate 
that the degeneration in the crossed motor tracts is of fihres that 
end lower down in the cord. There is no atrophy in the anterior 
horns or roots. The central canal is normal. Thoracic region.— 
In the first two metameres the sclerosis of the posterior columns 
has practically the same distribution, and is of about the same 
intensity as in the seventh and eighth cervical segments. The 
sclerosis below the second thoracic plane is slight and diffuse in 
the postero-median columns, except their most ventral parts. 
There is also a mild diffuse sclerosis of the median aspects of the 
postero-external columns. The eleventh and twelfth thoracic 
segments are, in addition to the above, slightly sclerosed in the 
position of the root zones and Lissauer’s tracts. No fibre atrophy 
or sclerosis is observable in the postero-internal zones, the comma 
tracts, or the cornu commissural zone. The lateral columns show 
a gradually increasing sclerosis as the cord is descended. As in 
the cervical region there is no rarefaction to speak of in the 
intermediate gray matter. Between the fourth and eighth 
thoracic segments the central canal of the cord is singular. It 
is irregularly cross-shaped, with short, transverse, and long, 
antero-posterior arms. The short arms pass off on each side 
between the gray commissures, and present a small bulbous 
dilatation at their extremities. The long posterior arm has pushed 
the posterior gray commissure backwards into the median septum 
for quite a fifth of the length of the latter. The ventral-ward 
extension has been turned to the left by the base of the anterior 
median fissure. Surrounding the enlarged canal is a thick layer 
of gelatinous substance. The cavity is narrow and free of the 
debris so commonly seen in the adult human cord. An even, 
compactly arranged layer of columnar cells lines the inner sur¬ 
face of the gelatinous substance. At first it was thought this state 
of the central canal was due to accidental distortion of the cord 
during removal. But the layer of columnar cells lining the cavity 
is compactly and evenly arranged, which could hardly have been 
so had there been an accidental heterotopia. Moreover, the canal 
is greatly dilated in the lumbar region, and has a projection back¬ 
wards capped by the posterior gray commissure, as in the thoracic 
region. It appears to be a developmental defect. Lumbar 



region.—There is a moderate, evenly distributed fibre atrophy and 
replacement sclerosis in the posterior columns of this region. It 
has scarcely affected the posterior aspects of the external columns, 
or the apices, composed of cornu commissural fibres. The fibres 
along the median septum are more closely arranged, and there is 
less sclerosis amongst them than in the rest of the posterior 
columns. The root zones and Lissauer’s tracts are slightly 
atrophied and diffusely sclerosed. In the roots external to the 
cord are a moderate number of partially wasted fibres. A few 
fibres have apparently wholly degenerated. In the lateral columns 
one may see a compact sclerosis of the motor tracts. It is much 
more marked than in either the thoracic or cervical regions. In this 
region there is a noticeable rarefaction of the intermediate gray 
matter. A few irregularly swollen fibres pass from the lateral 
columns into it. No wasted cells are to be seen in the anterior 
cornua. Sacral region.—This does not differ materially from the 
lumbar region. The sclerosis of the posterior columns is perhaps 
proportionately greater and more general. Charcot’s root zones 
and Lissauer’s tracts contain fewer fibres than in the lumbar 
segments. The extra-medullary portion of the roots are as in the 
lumbar region. The sclerosis of the crossed motor tracts is quite 
obvious to the naked eye, and is, under the microscope, fully as 
marked as in the lumbar region. The pia-arachnoid is slightly 
thickened between the points of entry of the posterior roots in all 
the levels of the cord. But there is no special concentration of it 
where the roots penetrate the cord. Throughout the cord the 
blood-vessels are slightly dilated and choked with red discs. 
In the patches of scar tissue the adventitia of the vessels appears 
to be slightly thickened. 

Case 62.— Tabo-paralysis , commencing with optic atrophy , followed 
by slight ataxy , defective hearing , auditory hallucinations , 
deafness , history of fits , transitory aphasia , affection of taste 
and smell. Medullary , optic and spinal tabes , slight changes 
in cortex cerebri . 

S. E. J., aged 32, admitted to Hanwell, February, 1896, on the 
following certificate:—“He is rambling and incoherent in his 
statements; says he hears voices at night, and they tell him he 
must get up. He is at times very excited and answers voices 
which are talking to him.” Occupation carman. The following 
history was obtained from his wife :— 



Family history .—Father deaf and dumb, died of asthma (?), 
mother alive in good health, one brother in good health. No 
history of insanity, intemperance or consumption in the family. 

Personal history .—He enjoyed good health up to six years ago, 
when he complained of pains in his legs. A little later his sight 
began to fail. This, however, did not prevent him from following 
his occupation for some little time. He attended the hospital in 
Queen Square under Dr. Buzzard, and the appended notes 
indicate his condition in April, 1893, showing that it was a case 
of optic tabes, in which the patient remained for some time in a 
pre-ataxic condition. He has been very temperate, and there is 
nothing in his occupation which might have led to his illness, 
with the exception that he has had boxes of oranges and potatoes 
fall on his head on separate occasions, once eleven years ago, and 
again seven or eight years ago. The brain affection appeared to 
have commenced twelve months ago with fits. 

The following are the notes of his condition when under 
the care of Dr. Buzzard, kindly supplied to me by the 

Admitted into “ Queen Square ” on April 11, 1893. For two 
years and five months, dimness of vision of left eye. For 
two years and three months, dimness of vision with right eye, and 
vision with left eye almost lost. For two years, vision with right 
eye almost lost. Lightning pains in lower limbs (? date). One 
year and nine months, unsteadiness in walking. Nine months, 
shooting pains in back of head, both sides. One month, shooting 
pains across front of chest. 

State on admission .—Gait slightly ataxic,, also movements of 
arms. Shooting pains as above. Tingling in hands and feet. 
Sensibility to touch, pain, and temperature, good. Knee-jerks 
absent, also other tendon reflexes. Sphincters, unaffected. Vision, 
bad, only movement of objects. Eight eye worse than left. Optic 
discs atrophic. Unequal pupils, loss of light reflex, nystagmus. 
Upward movement of both eyes and outward of left, defec¬ 
tive. Hearing, right, left, f. Bone condition better on right 

December 9, 1896.—He lies quite unconscious of everything 
around him. The attendant informs me that since I saw him, he 
has had many fits, which were more marked on the left side. 
Patient is greatly emaciated, and lies in bed with his legs drawn 
up, taking no heed of painful impressions, and apparently uncon¬ 
scious of his surroundings. When, however, food is placed near 
his lips with a feeder, he will suck at the spout, but does not 



seem to distinguish between milk and a strong solution of quinine, 
which he takes equally well. 

January 1.—Death from asthenia. 

Present state (February, 1896).—He admits having suffered 
with syphilis before marriage. Physical condition.—His gait is 
not ataxic. He can stand with his heels together and his eyes 
closed. He is quite blind. The pupils are unequal, the right 
dilated, the left contracted, neither react to light. He suffers 
with pains in his arms, and he cannot touch the tip of the nose 
with his right forefinger, or make the two forefingers meet. He 
is deaf in both ears, but can hear loud shouting. There is 
nystagmus when told to look towards his right hand. There is 
no tremor of the tongue or face, but a little hesitancy and slurring 
of speech. He says he lost power of speech for some time last 
July. Examination of the fundus showed white atrophy of both 
discs, vessels normal in size. 

Mental condition. —The memory is fairly good, but his intelli¬ 
gence is somewhat impaired. This may however be due to his 
blindness and deafness. He complains of hearing voices and 
sounds like bells ringing in his ears, especially at night. 

July 8, 1896. —Progressive physical and mental enfeeblement. 
Painful sensation blunted, likewise taste and smell. 

Abstract of notes of the autopsy from post-mortem book .— 
Pia-arachnoid opaque and thickened, especially over left angular 
gyrus. It is adherent to the brain substance in a few places. 
There is some congestion of the veins. Pia-arachnoid in the inter¬ 
peduncular space is greatly thickened. Optic nerves are gray and 
shrunken. The lateral ventricles are dilated, but apparently not 
granular. The fourth ventricle is dilated and granular. There is 
a clot of blood outside the membranes in the lumbo-sacral region 
of the cord. The liver is fatty. Hypostatic pneumonia of the 
right lower lung. 

Microscopical examination (by Dr. Hamilton Wright): Brain .— 
The tangential fibres are almost wholly absent from the mole¬ 
cular layer of the central gyri. Most of the proper cells of the 
cortex are extremely atrophied. Glia and spider cells are greatly 
augmented. Spinal cord.—Vessels congested, great numbers 
of leucocytes, walls of arteries thickened. Cervical region.— 
The posterior median columns show a marked scattered atrophy 
of fibres, about one half have disappeared ; those in situ are 
fairly sound. On the outer side of each intermediate posterior 
septum is a band of sclerosis containing only a few fibres, all in a 
state of chronic wasting. This sclerotic band extends backwards 


almost to the periphery of the postero-external columns. It is 
cut off from the commissure in its anterior aspect by fibres of the 
cornu commissural zone. Lissauer’s tracts on both sides are 
almost denuded of fibres, and they have been replaced by scar 
tissue. The root zones of Charcot are deeply sclerosed. External 
to the cord the posterior roots are almost wholly atrophied. 
Many fibres remain in the bases of the postero-external columns, 
i.e., in the position of the postero-internal zones. The fibres of 
the cornu commissural zones are almost intact. There is a 
readily observable atrophy of the plexus of fine fibres in the 
upper part of Clarke’s column. There is no atrophy of fibres 
in the lateral columns. Thoracic regions.—The greatest atrophy 
of fibres is in the root zones, and middle third of the postero¬ 
external columns. There is, however, as in the cervical region, 
a considerable scattered degeneration and replacement fibrosis in 
both postero-median columns. Lissauer’s tracts contain many 
healthy fibres, but a chronic atrophy of some of them is obvious. 
Outside the cord the roots contain only a few fibres. The cornu 
commissural zone and the descending comma tracts are pervaded 
by a slight sclerosis, and appear to have lost a few fibres. The 
great majority are present, however, and are healthy. The plexus 
of fine fibres around the cells of Clarke’s columns are few in 
number. There is no special fibre atrophy in the antero¬ 
lateral columns. Lumbar region.—Charcot’s root zones are 
greatly sclerosed, also the middle third of the postero-external 
columns. There is a marked scattered degeneration throughout 
the postero-median columns. Most of the fibres in situ lie close 
to the median septum. The latter feature is well marked in the 
lower lumbar regions. The fibres of the cornu commissural zone 
are present in large numbers, and are mostly sound. In the roots 
external to the cord there is considerable atrophy of fibres, but 
this is not nearly so marked as in the cervical and thoracic regions. 
The posterior spinal ganglia contain many cells in a state of fatty 
degeneration; others are excessively pigmented and devoid of 
chromophilous granules. The cell capsules are markedly thickened. 
There is a marked sclerosis of the substantia gelatinosa centralis 
about the central canal of the spinal cord, in the first cervical 
segment, and where it opens out to form the calamus scriptorius. 
The floor of the fourth ventricle is likewise sclerosed, up to about 
the level of the striae acusticae. The post-pyramidal nuclei show 
changes. A few cells appear to have wholly atrophied, and most 
of those in situ are shrunken and closely embraced by the re¬ 
placement sclerosis. There is total atrophy of the plexus of small 



fibres, and of most of the larger fibres, that usually surround or 
penetrate the nuclei. A marked atrophy is observable of the 
internal arciform fibres and fibrse rectse, and there is a noticeable 
substitution sclerosis in the raphe. On both sides the nucleus 
arciformis is denuded of fine fibres, and its cells are shrunken. 
None of them, however, seem to have disappeared. In the corpus 
restiforme there is a slight diffuse sclerosis, with more marked 
islets here and there. It is possible that this is due to an atrophy 
of the continuations of the wasted arciform fibres. There is an 
almost entire absence of fine fibres from amongst the cells of the 
tenth, eleventh, and twelfth cranial nuclei. It is difficult to decide 
if there has been an actual destruction of any cells. Those present 
are shrunken and closely surrounded by an increased amount of 
sclerotic tissue. The degeneration in the intramedullary portion 
and in the stumps of the tenth pair of nerves is striking, but it is 
more marked on one side than the other. About one third of the 
more deeply implicated nerve has wholly atrophied. The com¬ 
plete atrophy of fibres is not so marked on the opposite side. 
Many of the fibres still present on both sides are irregularly 
swollen. In both the stumps and intramedullary portions of the 
nerves there is a considerable replacement sclerosis. As the 
hypoglossals pass ventral-wards to escape from the bulb, and in 
the stumps of their trunks, a few degenerated fibres may be 
observed. One of the most interesting features about this ease is 
the atrophy in the nucleus ambiguus, or accessory vagal nucleus, 
and the solitary fasciculus on "both sides. In the nucleus on both 
sides there is a marked atrophy of the fine plexus of fibres amongst 
the cells and of the fibres that compose the stalk. The more 
deeply implicated nucleus and stalk is on the same side as the 
more atrophied tenth nerve. Beyond doubt the marked atrophy 
in the tenth nerve is in part due to the atrophy of those fibres of 
•the accessory vagal nuclei which enter into their formation. The 
vertical fibres of the solitary fasciculi are obviously wasted on one 
side only. On both sides the plexus of fine fibres in the sur¬ 
rounding gelatinous gray matter are wasted, almost wholly on the 
side where are the atrophied vertical fibres, and moderately on the 
side where the vertical fibres are intact. The more degenerated 
fasciculus is on the same side as is the least affected accessory 
vagal nucleus. Strands of fibres pass from both fasciculi to the 
intramedullary trunks of the tenth pair of nerves. They are not 
obviously wasted. In the ascending roots of the fifth pair of 
nerves there are a few wasted fibres and a moderate amount of 



Case 63.— Optic atrophy and blindness at 28, preataxic stage 
eighteen years , ataxy for a long time , preceded by mental 
symptoms , several fits, hallucinations , and delusions of perse¬ 
cution, progressive dementia . 

J. M., aged 48, metal polisher. Wife has known her husband 
since the age of 18. Patient’s mother died suddenly of a paralytic 
fit. He was very unsteady before the age of 21, when he 
married.’ Since his marriage, patient has drank. A son was 
born twelve months after marriage, and his wife had a miscarriage 
two years afterwards, and no children since. The son was 
healthy, but died aged 22, of diphtheria. At the age of 28 
(1880), patient began gradually to lose his sight, and he became 
completely blind in about twelve months. The doctors told him 
that he had “ white atrophy.” At this time he was mentally 
unstable. During the last two years (1898-1900) patient’s legs 
have seemed to give way under him a little. He used at different 
times to pray, swear, &c., but never wandered from home. He 
finally squandered his money and “ should not have had the 
handling of it for a long time before this.” Patient had a fit in 
December, 1898, and was admitted to Bethnal House, from 
which institution he was discharged in September, 1899. He was 
at home for five weeks, and during this time whilst in a fit “ put 
his head through a pane of glass ” He had weakness of the 
right side, and was very shaky afterwards. Before he had been 
at home a fortnight “he began to be afraid, and wanted to go 
back to the asylum.” He was admitted to Clay bury on November 
S, 1899, and was certified as follows : “ Aspect vacant and smiling, 
quite incoherent, does not know where he is, can give no account 
of himself, wishes to die, answers imaginary voices, has been 
noisy, shouting ‘murder’ and ‘ police,’and saying voices accuse 
him of stealing.” On admission, the speech, tongue, lips and 
facial muscles were tremulous, the pupils were fixed and irreg¬ 
ular, the right being slightly the larger, he was quite blind, and 
slightly deaf, and the knee-jerks were absent. He was depressed 
and very emotional when spoken to, he had delusions of persecu¬ 
tion, and said people were trying to poison him. He was very 

Further notes .—March 21, 1900.—Knee-jerks absent, sensa¬ 
tion apparently normal, stands and walks very well for a blind 
man, pupils irregular and immobile, 3 mm., the right slightly 
the larger, slight wobbling nystagmus, white atrophy of discs, 
memory very good, knows the day and year on which he was 



born, his age, period of blindness, &c., and says he has been here 
twenty weeks all but two days. Knows the present date, &c. 

October 23, 1900.—Knee-jerks absent, hypotonus to within 
20° of the vertical, right pupil very irregular, and left 
somewhat irregular. They vary in size around 3 mm., some¬ 
times the right and sometimes the left being the larger. The 
speech is tremulous and jerky, and drawling and typical of 
general paralysis. The tongue is very tremulous, there is right 
facial paralysis, and the right hand is slightly paretic. He is 
exceedingly dull mentally, and anxious to go home. 

November 16, 1900.—There is hypotonus to within 15° of 
the vertical in both legs. The right pupil shows most irregularity, 
and is slightly the larger. There is marked tremor of the tongue 
and face, and the speech as before is typical of general paralysis. 
There is some right facial paresis, but no weakness of the arms. 
He is very active on his legs considering his condition. He feels 
“ all right ” and happy. He remembers quite well recent and 
remote events, and the present day and date. He knows “ as he 
has a memory.” He is very impatient of control, and dislikes 
being examined as “ he is blind, and it is therefore unnecessary.” 

January 4, 1901.—He is now an advanced general paralytic, 
both the pupils are irregular, the right mm. and the left 3 mm. 
He is now very feeble and cannot stand or walk. He sits all day 
in a chair rubbing his hands over his head, or one hand against 
the other (he was a metal polisher). To questions, he drawls, 
“I’m all right,” or “I forgits,” he is restless and irritable if 
interfered with, wet and dirty in his habits, and quite helpless. 

February 10.—Death. 

Abstract of port-mortem. — Summary .—Gross signs of general 
paralysis with sub-dural haemorrhage, old-standing optic atrophy, 
syphilis probable but not positive, bladder hypertrophied, acute 
cystitis, broncho-pneumonia. 

Morbid histology. —Microscopical examination of the brain by 
Nissl and other staining methods for showing fibres exhibited the 
ordinary characteristics of advanced progressive paralysis. The 
spinal cord and cauda equina were examined by the Weigert and 
Pal methods. (1) Cauda equina.—Marked congestion of veinsother- 
wise no change in the vessels or their roots. Diffuse atrophy an 
denudation of fibres in nearly all the bundles, both anterior and 
posterior but especially of the latter. Some degree of substitu¬ 
tion fibrosis but not equal to the atrophy. (2) Second sacral and 
surrounding roots.—Atrophy of attached posterior roots, diffuse 
degeneration of exogenous fibres in posterior columns and cornua. 


escape of endogenous fibres. Slight sclerosis in crossed pyramidal 
tracts. (3) Fourth lumbar.—Ditto. Crossed pyramidal degenera¬ 
tion much more marked; anterior roots show no obvious atrophy; 
posterior roots, on the other hand, fairly marked atrophy, one-third 
to half the fibres gone ; diffuse but pronounced degeneration with 
neuroglia substitution of exogenous systems, with escape of the 
endogenous; anterior horn cells unchanged except for some chro¬ 
matolysis. (4) Tenth dorsal.—Slight degeneration of posterior 
roots, more marked on one side. Slight atrophy of fibre plexus of 
Clarke’s columns, degeneration and atrophy of fibres in middle 
of postero-external column, and of fibres proceeding to form Goll’s 
column, viz., middle and long fibres are degenerated in proportion 
to affection of the posterior roots of the lumbo-sacral region. There 
is some atrophy of Lissauer’s tracts proportional to the atrophy 
of fibres in roots. Eighth dorsal.—Ditto. The pyramidal tracts do 
not appear to be so obviously sclerosed as in the lumbar region. 
Sixth dorsal.—Ditto. Seventh cervical.—No degeneration of 
posterior roots, diffuse degeneration and sclerosis of Goll's 
column, slight degeneration and light diffuse sclerosis in tract 
lying outside of Goll’s column and corresponding to fibres from 
first dorsal and eighth cervical. No obvious degeneration of 
pyramidal tract commensurate with what is seen in the lumbar 
region. Second cervical.—Ditto. No obvious degeneration of 
direct tract at this level or elsewhere. 

GROUP 6.—Coi^jugal Tabes and Paralysis. 

Case 64.— Conjugal tabic general paralysis, history of injury to head 
when a child , damage of prefrontal region of left hemisphere. 
Illness commenced with optic atrophy and blindness , followed 
by visual and auditory hallucinations , delusions , ataxy of 
arms , and progressive dementia. Death from acute attack of 
recurrent dysentery. A large depression dtie to loss of sub¬ 
stance of anterior portion of second and third frontal convo¬ 
lutions left hemisphere. Typical appearances of general 
paralysis of brain . Naked eye sclerosis of posterior column. 
Atrophy of the optic nerves. 

M. M. C., widow, aged 38. Admitted to Claybury, June, 1901. 
Husband, a soldier, latterly worked as carrier, who had fits, and 
finally went out of his mind and died in Shoreditch Infirmary. 
She was married a long time ago while she was in service. 
She has had no children and no miscarriages. She says that she 
has had a lot of trouble. Between 6 and 7 years of age she had 
a fall from the balcony, and there is a depression the size of a 



shilling on the forehead If in. above the centre of the left orbit. 
Her memory is very bad. She has had a feeling of a tight belt 
round her waisfc, and still possesses it. She has been unable to 
unbutton her clothes for some time past. Her speech is hesitant 
and slurred, there is slight tremor of the facial muscles, also 
slight tremor of the tongue. She says that she has had several 
times attacks of sickness. Pupils 6 mm., regular, inactive to 
light and pain. White atrophy, with cupping of both discs, 
vessels normal in size. Expressionless face, except when talking, 
when she is frequently moved to tears or laughter; she is very 
restless and difficult to examine. Continuous restless movement 
of the hands; no fits, says she has wasted. Knee-jerks 4- + 
right side, absent left side, plantar reflexes 4- epigastric 4- 4-, no 
hypotonus in the legs. Skin sensibility.—Very difficult to test, 
apparently hypalgesia from third to the seventh segments inclu¬ 
sive. Some loss of power of localising, as she does not always put 
her finger accurately on the spot pricked or touched. Says that 
she has frontal headache, sometimes very bad. She has had a 
deal of worry. She does not care about food much, and is 
troublesome about it. Urine normal, temperature subnormal. 
She is very restless- at night. The certificate stated that she was 
restless at night, and believed people came into her bed. She 
hears voices. 

History of patient (from mother).—Her daughter was married 
twelve years ago; the husband had been taken to Shoreditch 
Infirmary because he was out of his mind, he was too ill to move 
to an asylum, and he died there. She believes that his mental 
complaint was brought on by worry, owing to his wife becoming 
blind, and his losing his place at Carter Paterson's. He had been 
a long time in the army prior to marriage, and had served in the 
Artillery. He had been to India, and was said to have had sun¬ 
stroke there. For years previously to his death he had been 
irritable, but after his wife becoming blind, he had treated her 
kindly. He was a teetotaler for years, but latterly had occa¬ 
sionally broken out in drinking. He had latterly several fits. 
There is no history of insanity in the patient's family, with the 
exception of religious craze (revivalism) in the grandmother; she 
was not, however, put into an asylum. 

Dr. Macmillan informs me this patient was the subject of 
visual and auditory hallucinations. 

During her stay in asylum her mental condition was one 
of depression. She rarely spoke to anyone ; she was very sus¬ 
picious, and had delusions of persecution. She would do nothing 



she was told, had to be dressed and had to be fed, as she 
believed her food was poisoned. She frequently complained of 
feeling “ bad smells/’ and would often pull her clothes tightly 
round her and remark, “ I’m in such a mess.” She always com¬ 
plained of being dirty, and wanted to be washed. During the 
first three months of her stay here, she had the delusion that 
she was pregnant, but latterly seemed to have got rid of it. In 
January, 1902, she was transferred to the hospital for nine days, 
as she was suffering from an attack of dysentery. While there 
after the first two days she was much brighter, and developed 
the delusion that she possessed a large fortune. At the same 
time she was noticed to converse with “ voices.” She would sit 
up suddenly in bed, open her eyes and gaze at the ceiling, and, 
stretching her arms out, would say, “ I am coming.” She would 
often call on “ Harry,” and remark, “ I will be with you soon.” 
At times during her imaginary conversations, she would burst 
out laughing, as if amused by something she had heard. When 
allowed up, she would sometimes get up and walk across the 
ward, because she heard some one calling her to do so. If any¬ 
one spoke to her, she never turned her head towards them, but 
gazed up straight in front of her. 

Abstract of post-mortem notes .—Patient died on April 15,1902, 
eleven days after admission to Hospital from an attack of acute 
dysentery. The certified cause of death was, “ Acute dysentery 
supervening on chronic.” 

Main facts of interest .—No external signs of syphilis on the 
body. Scar, the size of a threepenny piece on the cervix uteri 
close to junction with vagina which might have been the result of 
a primary sore. There was a hole the size of a sixpence in the 
region of the left frontal eminence closed by dense fibrous tissue 
to which the dura and pia is adherent. On removal of the brain 
the dense fibrous tissue had to be cut through and it was found 
there was a considerable loss of brain substance in the anterior 
part of the second and third frontal convolutions, the cavity 
extending nearly to the orbital surface of the lobe; it was large 
enough to have held half an ounce of fluid. There is almost 
generalised thickening and opacity over the pia-arachnoid of the 
anterior two-thirds of the hemispheres." There is some wasting 
of the convolutions in these regions. There is not much dilatation 
of the lateral ventricles. Ependyma granular, fourth ventricle 
very granular, especially about the calamus. After hardening in 
Muller fluid, naked eye degeneration of the posterior columns of 
the cord, with moderate atrophy of the posterior roots, especially 



the lower cervical and upper dorsal, and lumbo-sacral. Marked 
gray atrophy of both optic nerves. Sections stained by Weigert 
method showed the usual degeneration of posterior roots and 
posterior columns of an early case of tabes. 

Case 65.— Conjugal paralysis.—Husband syphilitic, wife married 
twice, no children by second husband ; the former died of tabo- 
paralysis, the latter a short time after of ordinary paralytic 

G. S., aged 43, docker, admitted to Cane Hill Asylum, July 19, 

History. —Patient became gradually blind about two years ago, 
and subsequently suffered with locomotor ataxy, which took him 
to Stoke Newington Workhouse, where he remained one year. 
He then developed an attack of acute mania, becoming restless, 
excitable, and violent, threatening to stab another patient; he was 
certified insane. On admission to Cane Hill it was found that his 
wife was already in the asylum suffering from general paralysis. 
The following facts were elicited from friends: He did not drink, 
nor was there obtainable any hereditary history of insanity. He 
lost his sight gradually, and this was followed by drooping of the 
left eyelid, his mental state denoted considerable dementia and 
loss of memory, with defective knowledge of time and place; he 
has no delusions of grandeur or persecution, but is restless, noisy, 
and delirious, and although blind, has frequent visual hallucinations. 

Physical condition. —He has a fatuous expression, the face is 
congested, the skin greasy and there is incomplete ptosis of the 
left eye (see photo., fig. 37). The pupils are unequal, dilated and 
irregular; there is primary optic atrophy of both discs and there 
is tremor in the lips and tongue, but not marked; the speech 
is somewhat hesitant and slurred; his gait is shambling; he 
brings his heels down first and he walks with a wide base, but 
there is no marked ataxy; the knee-jerk is present on the right 
side, absent on the left. He is too demented to give any reliable 
answers in regard to cutaneous sensibility ; there are well-marked 
signs of syphilis on the body in the form of a scar on the glans 
penis, enlarged inguinal and cervical glands and tissue paper 
scarring all over trunk and limbs. 

When asked about his wife, he says he does not know where 
she is and doesn’t want to; she was brought to see him and she 
was much affected, but he was quite indifferent and told her to go 
away; he became more demented and died in December, 1899. 



B.S., his wife, aged 39, had one child by her first husband, but 
no children by her present one ; her illness began with a fit a short 
time before admission; she was taken to Guy’s Hospital and 
thence to the infirmary, has had no fits since. 

Mental condition .—She exhibits considerable dementia and is 
depressed, especially about her husband; the photograph shows 
this in her expression as compared with that of her husband. 

Physical condition .—Pupils equal, react to light sluggishly; 
react well to accommodation. She can walk about, tries, though 
feebly, to make herself useful in the ward. Tremor of the tongue 
and lips, and slight paresis of the right side of the face. Speech 
is very tremulous and syllabic. Knee-jerks exaggerated both 

Fig. 37. 

The physiognomy of the man denotes mild exaltation and dementia, that 
of the woman slight depression. 

sides. The disease progressed, patient becoming gradually more 
demented ; the tremor and speech affection more marked. The 
mental depression gave place to mild exaltation, and eighteen 
months after admission she died from exhaustion, following 
epileptiform seizures. 

Post-mortem notes (abstracted).—An old scar found on the out¬ 
side of the right thigh (? gumma), and cicatrix on the cervix uteri 
were the only signs which could possibly indicate syphilis. Body, 
well-nourished; brain, dura mater, non-adberent; considerable 
amount of fluid in sub-arachnoid space. Left hemisphere weighed 
14 ozs., right hemisphere weighed 17J ozs. The wasting of the 



left hemisphere was especially marked in the prefrontal and 
central convolutions. The same applies to the right, but less 
marked. The pia-arachnoid is thickened, adherent, and opalescent. 
Both lateral and fourth ventricles are granular, and the left ven¬ 
tricle is much larger than the right, corresponding to the difference 
in weight of the hemispheres. There is early atheroma of the 
aorta, but the cerebral vessels are normal. 

Post-mortem of G . S. (husband). —Died five months after 
admission. (Abstract.) Brain; pia-arachnoid thickened, especially 
over the frontal and central convolutions. atrophy of the left 
superior parietal lobule. Over the inferior surface of the orbital 
lobes on both sides, the brain substance, and the pia-arachnoid 
covering it, has an appearance not unlike that of a cirrhotic 
liver; on the mesial surface and tips of the prefrontal lobes, 
there is marked pia-arachnoid thickening and wasting of the 
convolutions. The lateral ventricles are not much dilated; the 
ependyma is somewhat granular; the fourth ventricle is dilated 
and very granular; Broca’s convolution shows very little wast¬ 
ing ; the pia-arachnoid strips with few erosions, the gray matter 
of the cortex is diminished, and in the lower part of the central 
convolutions the cortical striae are ill-defined. Both optic nerves 
are greatly wasted. Left hemisphere weighs 19 ozs., right 19| ozs. 
Pons medulla and cerebellum 7 ozs. Aorta was markedly ather¬ 

Death was caused by gangrenous pneumonia. 

Microscopical examination of the brain (by Nissl, Marchi, 
Marchi-Pal and Weigert methods).—Sections were taken from (1) 
ascending parietal, (2) second and third frontal, and (3) orbital. 
Summary of results .—The changes are mostly of a chronic 
degenerative character in all the areas examined ; few cells were 
acutely changed. The most marked acute changes in the cells 
are in the orbital region, where the vascular changes in the form 
of stasis and perivascular cell proliferation are most pronounced. 
The neuroglia cell proliferation is nowhere very marked. Becent 
degenerated radial fibres are seen in the central convolution by 
Marchi method, but none in the tangential or supraradial fibres. 
By Marchi-Pal and Weigert methods these layers of superficial 
association fibres are greatly diminished or absent in all those 
regions examined. The changes correspond to an ordinary slowly 
progressive case of dementia paralytica. 

'Examination of the spinal cord, ganglia and roots (by Marchi, 
Weigert-Pal, and Nissl methods).—By the Marchi method, sections 
of the cord in the cervical region at different levels showed a large 


number of degenerated fibres scattered about in the posterior 
columns, also in the crossed pyramidal tract on the right side and 
the direct of the left, showing that there was a recent degenerative 
process occurring in the brain. 

Different levels of the cord in the cervical, upper, middle, 
lower dorsal and lumbosacral regions were examined by the 
Weigert-Pal method. Sclerosis of the right crossed pyramidal tract 
and of the whole posterior median column was found in the 
cervical region. In the dorsal region there was degeneration 
in the postero-external column corresponding to Charcot’s root 
zone. This was especially obvious below the eighth dorsal. It 
seemed in this region that the degeneration and atrophy of fibres 
was more obvious on the side opposite the degenerated pyramidal 
tract. The sections were cut to include the roots, and sections at 
one level would show far more degenerated fibres in the roots 
than at another level. The degenerated roots would be sometimes 
more apparent on one side than the other. Lissauer’s tract 
generally showed diminution of fibres, but it varied at different 
levels. In the lumbo-sacral region, sections showed atrophy and 
denudation of fibres throughout the posterior column, except in 
the oval area of Flechsig and the cornu commissural zone. As in 
the dorsal region so here, the atrophy and sclerosis of roots is the 
subject of considerable variation, and is nowhere complete. 

Spinal ganglia (stained by Weigert method) cut in series.— 
The cells show in great part some protoplasmic change, for they 
have a blue appearance owing to the presence of fine stained 
granules. The nerve-fibres leaving the ganglion show considerable 
atrophy and sclerosis. In the capsule of the gland, and in the 
distal roots, a number of bundles of fine medullated nerve-fibres 
are seen, which are either deficient in fibres or are unstainable. 
The third lumbar, stained by Nissl method (serial sections of this 
ganglion being made).—All the sections showed a variable number 
of cells presenting change from slight chromatolysis to a very 
marked condition of the same. In many of the cells the nuclei 
are eccentric and hardly stained at all. 

Vascular and meningeal changes.—The changes in the 
meninges are not extensive, and although they are somewhat 
thicker over the posterior column of the cord, still there is not a 
marked flattening as is found usually in a prolonged chronic case. 
Notohere could a process of endarteritis be seen, and the 
thickening of the vessels would in no way explain the atrophy of 
the fibres. The sections of the cauda equina show that the vessels 
in the undegenerated anterior roots were as often thickened as 



those in the posterior, and in no case was an artery found blocked. 
Congested veins were found equally in both degenerated and 
undegenerated roots. 

The retinae and optic nerves were cut in celloidin and stained 
by logwood and eosin, by Strobe and Weigert methods. 

The retime exhibited no inflammatory changes or alteration of 
the vessels. The ganglion cell and nerve-fibre layers were entirely 
absent. The rods and cones were not distinguishable, but there 
was undifferentiated protoplasm, stained with the logwood, lying 
between the hexagonal pigment cells and the granular layers, 
which are intact. The sustentacular fibres of Muller were very 
distinctly seen owing to the absence of the ganglionic layer. 
There was considerable excavation of the papilla. 

The optic nerves were shrunken to half the normal size. The 
nerve-fibres were absent, their place being occupied by a fine 
meshwork containing a large number of round and oval granular 
nuclei or cells. The interstitial septa are thicker and more obvious 
than usual, and contain also a number of proliferating cells or 
nuclei. The vessels show no apparent change or only slight 
thickening of their walls. 

Case 66 .—Conjugal paralysis. Husband suffered with fits, hemi- 

paresis, and dementia, sluggish pupils ; diagnosed by Dr. 

Bailey and Dr. Alexander as probable general paralysis. 

Wife admitted with acute mania and died of tabo-paralysis. 

L. H., aged 54, admitted to Hanwell, January 11,1901, suffering 
with acute restless mania. 

History (from daughter).—Worried about her husband’s 
illness, and for the last two years has been strange, easily 
excitable and always talking about her troubles. The husband 
had a fit two years ago, since then unable to do any work, and 
this preyed on her mind. Two months before admission she had 
a fit followed by left-sided hemiplegia of a transitory character, 
she remained in bed three weeks, after this she was able to walk 
about as before. She then became restless and strange, getting 
up in the night to hide things, wanting to buy all manner of 
things, going out of doors and talking to strangers about the way 
people treated her, untidy in her dress and dirty in habits. 

When I saw her four days after admission she was in a state 
of acute mania resembling alcoholic mania, but there was no 
history of intemperance. There was a history of three successive 
miscarriages, and the notes state of syphilis. This was probable 



from statements made in her delirium. She kept repeating, “ he 
poxed me—my son must be cut like a Jew.” She says she dreams 
all manner of things, she sees Old Nick. She says that they have 
put poison in her feet, legs, and arms. She says burglars came 
into the house, they boiled the pot and then poured it down her 
throat. She thinks she is at Crawford Street still. She is 
going to be married and wants clothes of gold. She does not 
recognise the nurse or doctor. She has not been to the closet for 
three months ; the food is poisoned. Continuous restless motile 
delirium, and tears up her clothes. Sings and shouts and hardly 
sleeps at all while in the padded room. She was brought to the 
asylum tied on a stretcher. 

Physical condition. —Emaciated, no teeth, knee-jerks absent, 
tenderness of the calves when compressed, pupils unequal E. > L. 

mm., 4 mm., speech a little slurred and hesitant. 

March 17.—Mania still, but not so marked, yet restless, 
excitable and full of delusions about valuable ornaments and gold 
watches, frequently takes her clothes off, and is very trouble¬ 
some. Arteries atheromatous; aortic regurgitation, collapsing 
pulse, acute mania of general paralysis diagnosed. 

March 28.—Mania subsiding, orientation in time and place 
very imperfect. No tremor of tongue, articulation fair. Pupils 
irregular, dilated, equal inactive to light, sluggish to accommoda¬ 
tion. No tenderness on pressure of legs. Knee-jerks absent. 
She now knows her friends and talks to them, but memory very 

October 30.—She is now a well pronounced general paralytic. 
Dr. Bailey saw Mr. H., the husband, 1 he is partially demented, 
pupils unequal, sluggish reaction to light, speech slow and 
hesitant; history of several paralytic seizures. Dr. B. considered 
that the patient was a general paralytic. 

November 28.—Much weaker, confined to bed; sometimes 
hardly speaks for weeks together. To-day she was more talka¬ 
tive. Knee-jerks absent. Triceps-jerks easily obtained. Lies 
in bed with hips and knees semi-flexed, but feet plantar-flexed and 
somewhat inverted. She does not take any notice of sharp prick¬ 
ing of the legs, nor of a strong faradic current, but she immediately 
does when the arms are stimulated or pricked. All the muscles 
respond to faradism. Plantar and epigastric reflexes obtained 
with great difficulty. 

December 6.—Eight-sided epileptiform convulsions. 

1 Subsequently I ascertained Irom a doctor who treated the husband that 
he had had syphilis. 



December 13.—Death. Pupils unequal, right 5 mm., left 6 mm. 

Post-mortem .—Body much emaciated. Left hemisphere sub¬ 
dural haemorrhage about one week old. No naked eye softenings* 
Right hemisphere 18 ozs., left 18 ozs., cerebellum and pons 
5 oz. Sub-arachnoid fluid increased. Ventricles somewhat dilated, 
granular ependyma, especially lateral sacs of the fourth ventricle, 
Pia-arachnoid thickening over frontal and central convolutions 
especially. Some atrophy of convolutions. Typical appearances 
of early general paralysis. Aorta atheromatous second degree, and 
aortic valvular incompetence. Spinal cord—after hardening in 
Muller—showed well-marked posterior and lateral column de¬ 

Case 67.— General paralysis {tabetic), wife suffering from locomotor 
ataxy . Impaired cutaneous sensibility to pain on the left side 
after a series of epileptiform seizures . Death one year after 
admission . 

W. F., aged 38. Occupation journalist, admitted to Cane Hill, 
December 6, 1900, first regarded as an epileptic. He came from 
Lambeth Infirmary under the following certificate:—“ Strange 
in manner and states that he is starved here (a delusion); states 
he wants to goto South Africa at once before Roberts and DeWet 
finish; that he has the editorship of a leading paper there; says 
that he has a comfortable home there to go to, and plenty of money. 
The wife states that there is no home now.” There is no history 
of insanity, phthisis, or alcohol. He has been married nine years, 
no children, one child born dead eight or nine months after 
marriage, denies syphilis, but there is a scar on penis and indurated 
glands. His illness commenced two years ago with a fit. At the 
end of January the patient had a series of left-sided epileptiform 
seizures which according to the attendant began in the angle of 
the mouth and spread over the left side. He does not lose con¬ 
sciousness but becomes drowsy. I saw him in June, 1901, for the 
first time. The attendant informs me that the wife, who lives at 
Sheffield, had visited the patient and he had noticed that she 
walked with a characteristic ataxic gait, and she told him herself 
that she had suffered for some few years past from the same 
disease, locomotor ata»xy. Patient is lying in a semi-stuporose 
state being affected with a congestive seizure, so that he is 
incapable of examination. 

July 5.—Patient is now up and walking about. The following 
notes were made :— 



Physical condition .—There is no ataxia in his gait and he can 
stand with his eyes shut ; grasp good both sides, and there is no 
muscular weakness. No loss of sense of position in the hands or 
feet, superficial reflexes rather exaggerated, knee-jerks absent both 
sides, triceps-jerk and wrist-tap contraction easily obtained, no 
affection of speech or handwriting, tongue slightly tremulous, 
somewhat expressionless face except when conversing. Pupils 
equal, 3£mm., a little irregular outline, do not react to light or 
pain, react to accommodation. The last time I saw him the 
pupils were unequal, the left being the larger. 

No trouble with the bowels or bladder. 

'■ The attendant says that he has had several left-sided seizures 
since I saw him, which last about one and a half minutes* Ip 
one, the attendant saw him go to the left in falling “like a 
peg top.” Some hypotonus in the legs, rather more marked on 
the right than the left side. 

Sensory .—Cutaneous Sensibility.—All over the left arm and 
leg and left side of trunk are spots in which prick of pin is not 
felt, or only as a touch ; there are also spots of tactile anaesthesia. 
He was tested in the following manner, stripped and eyes blind¬ 
folded. He was told to touch with his finger the part pricked or 
touched. This he invariably accomplished accurately and without 
delay on the right side, not so, however, on the left. Sometimes 
he localised wrongly, sometimes he did not feel at all the prick of a 
needle or touch with finger. There was no precise root area deter¬ 
minable except over the left buttock and around the anus on the side 
that the defective sensibility was most marked. No loss of joint 
sensation could be determined. He has no hemiparesis. Smell 
and taste.—Thinks asafoetida smells like violets, cannot smell rose 
water or strong peppermint. He did not recognise acids, salines, 
or syrup, but recognised bitters when quinine was painted on the 
back of the tongue. There is no limitation of the field of vision, 
and his colour perception is good enough to pick out the ordinary 
colours. Hearing.—Hears a watch at 18 ins. from both ears. 

Mental State (October 15).—Patient is fairly coherent, except 
when suffering with conjestive seizures. He has had hallucinations 
of vision, seeing people lying alongside of him and annoying him. 
He is said to have had delusions with regard to his bowels. He 
can give a fairly rational account of himself, and I could find no 
gross loss of knowledge of time or place. He says that he has had 
no pains in the legs and no feeling like a cord round the waist. 

January 13.—Death took place. 

The brain showed well marked signs of general paralysis in the 



first stage. First stage of sclerosis in posterior column. Wife 
was seen by Dr. Cribb, and he found her to be a well-marked case 
of locomotor ataxy. She had attended Queen Square for some 
years for this complaint. I wrote asking her to come and see 
me, but she did not turn up. 

Case 68 .—Conjugal tabo-paralysis of an aged couple (the melan¬ 
cholic type). Wife affected after the husband, rapid course of 
the disease in both cases. 

E. E. G., admitted to Claybury, December 14, 1900, died 
October 19, 1901, aged 64 years; occupation washerwoman, 
moderate drinker. 

Family history incomplete, husband a carpenter in Woolwich 
Arsenal, afterwards pensioned, was several years in the Volunteers, 
died in Banning Heath Asylum, July 26, 1899, after two years 
and four months residence, aged 64 years. Had two fits before he 
went away, and one later. He went blind while he was in the 
asylum, he was said to have “ paralysis of the brain,” or “ general 
paralysis.” Patient was married forty-five years, she had in all 
eighteen certain conceptions, two boys and five girls are alive and 
healthy. She had at least five still-borns or miscarriages, all the 
rest died as babies. 

History of attach .—Patient grieved very much when her 
husband was taken to Barming Heath, but she kept fairly well 
mentally for some time. Twelve months before admission she 
became suspicious and strange in her manner; “ one time said 
she was not at home and got her things, and said she was going 
home,” very restless at night, began to “ talk funny and say 
senseless things,” used to hear voices about. If she had money, 
“ they never knew where it went ”; she thought “ robbers were 
getting into the house,” and “ there was a cellar below, and 
children were crying in it.” She could not be left alone; “ one 
night she got out and had a clock under her arm and a cup of tea 
in her hand, and said she was going home.” Her husband had 
been a very similar case, and as he had done, so used she to cry for 
hours at a time, and say that everyone was hard on her, and no 
one did anything for her, and also that she never had any money, 
and was not at home. Some months later she fell down in the 
back garden, and could not speak for twelve hours, but seemed to 
have no paralysis. She was then in bed for about six weeks. 
After this she was up for about a month, during which time she 


began to wander about as before, or worse, and finally was sent 

Certificates .—Very talkative, restless, and incoherent, is con¬ 
stantly getting in and out of bed at night, wandering about, talking 
to imaginary persons, and quarrelling with other patients and 
pulling them about. 

On admission .—Serpiginous ulcer on outside of right knee 
(diagnosis syphilitic), scar on left leg, bronchial rales in chest. 
Memory much impaired, depressed and miserable, gives a confused 
account of her past life, sees strange persons about her bed, wet 
and dirty in her habits. 

January 3, 1901.—Knee-jerks absent, right pupil 2, left If, 
they accommodate to If and If, right (?) irregular, left irregular, no 
reaction to light, very little tremor of tongue, speech not char¬ 
acteristic, talks rather sensibly but is demented, is occasionally 

March 10, 1901.—Brighter but memory remains defective. 

September 10, 1901.—Palate high, teeth very good for age, 
considerable tremor of tongue, voice very tremulous and hesitant, 
and characteristic of general paralysis, right pupil 2f, left 2 
minus, accommodate to 2 and If, both knee-jerks absent, left foot 
has a sore on the outer malleolus, and is redder and colder than 
right. The ulcer on the outer part of the right knee has healed 
leaving a serpiginous pigmented scar. Patient is in bed and very 
feeble. She is very emotional and cries when her husband’s 
name is mentioned. She remembers my face though she has not 
seen me for eight months.—(F. W. M.) 

4 October 19, 1901.—Died of exhaustion. 

Post-mortem .—External appearances as described above. 
Skull.—Considerable hypertrophy of inner table in frontal region, 
and dural adhesions. Eight pupil 4 mm., left 3, no definite signs 
of optic atrophy, but the left is a little smaller and grayer than the 
right. Great excess of subdural fluid. Pia-arachnoid, there is con¬ 
siderable fronto-parietal thickening and milkiness, much congestion, 
sub-pial extravasations on right pre-frontal region and scattered 
over left frontal region. Mid-line pre-frontal adhesions, which 
decorticate on stripping, slight excess of sub-arachnoid fluid, basal 
vessels much dilated, and internal carotids highly atheromatous. 
Weight of encephalon 1380 grammes, right hemisphere 575, left 
580, cerebellum and pons 170. Moderate pre-frontal wasting, 
lateral ventricles much dilated and granular, third ventricle granu¬ 
lar, fourth ventricle granular throughout. The whole of the 
encephalon is congested and the sinuses are full of blood-clot. 



.Lungs emphysematous and oedematous, heart flabby and full of 
dark clotted blood, cavities dilated, mitral valves slightly athero¬ 
matous, one or two specks of early atheroma in coronary arteries, 
a relatively little amount of second stage atheroma in the aorta 
and a few pearly white patches* which are more frequent in 
the abdominal aorta than in the thoracic. Liver congested but 
otherwise natural except for a little scattered fatty degeneration. 
Spleen small and diffluent ; kidneys, capsule slightly adherent, 
congested, cortex 4-6 mm., density increased. Eenal arteries 
.considerably thickened, stomach catarrhal, intestines natural, sub¬ 
acute cystitis, uterus somewhat atrophic, ovaries and tubes 
extremely atrophied. 

. Cause of death. —Exhaustion of senile general paralysis. 

Microscopical examination of spinal cord. —Size fairly normal 
at all levels, no flattening posteriorly, only slight pia-arachnoid 
thickening. Slight diffuse atrophy in direct tracts both sides, 
most noticeable in the upper cervical region. The crossed pyra¬ 
midal degeneration is apparent to the naked eye in the lumbo¬ 
sacral region, but apparently diminishes as the cord is examined 
upwards. The exogenous fibres in the lumbo-sacral region are all 
markedly affected, and there is atrophy of the plexus around 
Clarke’s column cells. The posterior roots are also sclerosed, and 
partially denuded of fibres in this region. In the dorso-lumbar 
region there is considerable atrophy, but the short, fine fibres are 
less affected. In the mid-dorsal there is very little root-fibre 
degeneration. In the upper dorsal there is slight degeneration of 
posterior roots, and cornu radicular one. 

Copy of entries in Barming Heath case-hook respecting 
G.H. G: Date of admission.—April 12, 1897. Age and sex.— 
61 years, male. Friend.—E. E. G. (wife), 39, H. Road. 

Medical certificate ,(W. E. Boulter, April 10, 1897).—His 
speech is uncertain and hesitating, and he is generally tremulous. 
He says he has only been out of sorts a short time, is quite cheerful, 
and says he can still do his work all right, but people won’t take 
it when he has done it. (2) His wife, E. G., 39, H. Road, says he 
has been very strange for the past eighteen months, has delusions 
that he is going to die at once, lays himself out in bed and calls 
all his children to him. He is much upset by work being refused 
that he thinks he has done properly. 

, On admission .—Mind a blank. Has no idea of time or place. 
-Has no knowledge of where he is now, or where he has come from. 
Is happy and light-hearted, laughs stupidly like a drunken man, 
and says he feels as. happy as a dog. Physically well developed, 



well nourished. Lungs healthy. Heart irregular, aortic regurgi¬ 
tant murmur. Is very ataxic . Pupils irregular and do not respond 
to light. Speech thick and mumbling, will commence a sentence 
all right, then slur over half a dozen words, and finish off correctly. 
Knee-jerks absent, free from bruises. 

April 27.—No improvement, marked signs of general paralysis. 

May 14.—Advanced in general paralysis, much weaker. 

June 10.—Very weak and helpless, dirty. 

August 20.—Patient had a severe convulsive attack to-day. 

November 20.—Patient has picked up again, but very tottery. 

February 7, 1898.—He is getting much weaker, speech very 

March 8.—Very weak, advanced in general paralysis 

April 8.—Very weak and uncertain on his legs. Pupils widely 
dilated. General paralysis well marked and advancing, 

September 5.—Bapidly worse, hardly able to move. Very 
restless at night, generally sleeps in padded room. 

December 8.—Unable to move or help himself, destructive. 

June 27, 1899.—Very feeble and utterly helpless, no mind. 

July 26.—Sank and died this morning at 6.15 a.m. in the 
presence of Attendant J. Brooker, the probable cause of death 
being general paralysis of the insane. One bedsore on right 
shoulder, one in the middle of the back, and a slight one over 
sacrum. Notice of death sent to Coroner this day, of which the 
following is a copy: G. H. G., male, 63 years, married, wood 
sawyer, admitted from 39, H. Boad, died at 6.15 a.m., July 26, 
1899, of general paralysis of insane (not ascertained by post¬ 
mortem examination) in the presence of Attendant James Brooker, 
the duration of the disease being about three and a half years. 
Bed sore on shoulder and middle of back, no mechanical restraint. 
(Signed) F. Pritchard Davies, M.D., Medical Officer; Thomas W. 
Dadd, Clerk (Dated July 26, 1899). 

A post-mortem examination was refused (F. Pritchard Davies, 
M.D., Superintendent). 

Case 69.— Conjugal general paralysis in husband and wife . Definite 
signs of syphilis in the wife . 

E. C. B., aged 53, married; occupation, furniture dealer. 
Admitted to Clay bury, September, 1896, with delusions and auditory 
hallucinations; he threatened to murder his wife; there is no 
history of insanity or intemperance, he was married twenty years 



ago, and has one child. Exciting cause attributed to failure in 
business and family troubles. 

Condition on admission .—There is well-marked leucoplacia of 
tongue, indurated glands in the groin, but no evidence of a scar 
on the penis. He is in poor bodily condition, the knee-jerks are 
obtained with difficulty, but no ataxy noted, the pupils are said to 
be equal, and to react to light and accommodation. 

Mental condition .—He is talkative and incoherent, he complains 
of his wife's actions, and states that he wished to kill her and the 
boy. At times he has religious exaltation, and wants to die. He 
talks of his mother possessing a large property, and he is continu¬ 
ally making large profits out of the exchange and sale of furniture. 
His knowledge of time and place is most imperfect. Occasionally 
he is noisy, excitable and difficult to restrain. Diagnosis, mania 
of general paralysis. 

His general health improved in the asylum, and the symptoms 
of acute mania gradually subsided. About a year later a growth 
was found in the left half of the tongue which was called epithe¬ 
lioma ; one half of the tongue and the sub-maxillary glands were 
removed. There was no recurrence of the growth. As no micros¬ 
copical examination of this was made, it is open to doubt whether 
this was epithelioma; in fact, the history of leucoplacia, the syphilitic 
eruption and the syphilitic eruption on the wife, to be afterwards 
described, make it probable that it was a syphilitic gumma. The 
symptoms of general paralysis became more marked, tremor of 
the facial muscles, slurred speech, pupils inactive to light, and 
occasional epileptiform seizures with mental exaltation, firmly 
established the diagnosis. On October 12, 1898, he had an 
apoplectiform seizure followed by paresis of the left arm and leg, 
accompanied by pyrexia, 103° F. This is of interest in connection 
with the atrophy of the right hemisphere found post mortem. On 
November 13, 1899, he again had a seizure affecting the left side. 
It was noted that his speech was never much affected; in fact, 
the attendant says that his speech has never been any worse than 
one would expect in a man who had lost half his tongue. The 
right knee-jerk just present , the left markedly exaggerated , but no 
ankle clonus. Right and left triceps jerks exaggerated, all super¬ 
ficial reflexes increased. His mental and bodily condition 
progressively deteriorated, and he died on December 18, 1899. 

Post-mortem examination showed the following conditions :— 
Enlargement of cervical and inguinal glands, but no other signs of 
syphilis, no evidence of recurrence of growth in mouth. Brain.— 
Adhesions of dura mater to skull, pia-arachnoid thickening, which 



gives rise to erosions on stripping, marked wasting of the convo¬ 
lutions in the frontal region, and also of those along the vertex of 
the hemispheres adjacent to the superior longitudinal sinus. The 
right hemisphere weighs 90 grammes less than the left, the cortex 
is diminished, especially of the right hemisphere, and the striaB 
indistinct. The ventricles, both lateral and fourth, dilated and 
very granular. Weight of right hemisphere, 475 grammes, weight 
of left hemisphere, 565 grammes. Atheroma of aorta and coron¬ 
ary arteries, slight atheroma of cerebral arteries about base. 

E. R., aged 37, housewife, admitted to Cane Hill Asylum, 
October 13, 1897, died September 6, 1898. Mental disorder, 
dementia, with general paralysis, certified cause of death general 
paralysis of the insane. 

On admission the notes state that this patient was a fairly 
well nourished woman. She was suffering with a syphilitic, scaly 
eruption on the face and legs, and ptosis of the left eyelid, and 
had a vacant, emotionless expression. The pupils were unequal, 
right larger than the left, both inactive to light. Superficial and 
deep reflexes were increased, and the speech was hesitant, slurred, 
and indistinct, with tremor of the tongue and face muscles. 
Mentally she was dull and slow in thinking and answering ques¬ 
tions. Her memory and intelligence were much impaired; she 
had delusions, like her husband, about furniture, for she believed 
the ward furniture was all hers, and that she could exchange or 
sell it. The dementia progressed, and on August 25, 1898, she 
had an attack of left-sided epileptiform convulsions, which lasted 
for a few days; the condition became worse, and she died from 
exhaustion on September 6. 

Post mortem .—At the autopsy the dura mater was found 
adherent to the calvarium. The pia-arachnoid membrane thickened 
and opaque, adherent to the convolutions, which were atrophied 
and left erosions on stripping. The notes state there is consider¬ 
able softening in the left hemisphere, chiefly in the frontal and 
parietal lobes, and an appearance of red softening. (No note is 
made of the condition of the veins opening into the longitudinal 
sinus, but it is probable that venous obstruction or thrombosis 
was the cause, and there is no doubt that the left-sided epilepti¬ 
form convulsions, from which she had suffered just prior to death, 
were associated with and due to this condition). The right 
hemisphere weighed 18^ ozs., the left 21 ozs. No doubt an acute 
destructive process accounted for the marked loss of weight of the 
right hemisphere. The condition of the ependyma of the ventricles 
is not noted, but the lateral ventricles are said to be somewhat 



GROUP 7.—Ataxy with Non-Progressive (? Alcoholic) Dementia. 

Case 70.— Ataxy , alcoholism , syphilis , neuropathic family history, 
delusions of persecution and hallucinations, probably the result 
of alcoholism and heredity, dementia, which combined with 
the physical signs led to diagnosis of tabetic general paralysis. 
Mental symptoms greatly improved, also physical. 

T. N., aged 39, admitted to Claybury, August, 1896, formerly a 
soldier, then commercial traveller, then kept a coffee house. 
Married, four children, two died a fortnight before birth, other 
two at birth, full-time. Lived a very dissolute life, given to 
drunkenness and great sexual excesses, acknowledges syphilis 
contracted at Aldershot, 1883, well marked scar, enlarged glands, 
secondary symptoms (treated twelve months), followed two or 
three years later by loss of sight in right eye. His wife states 
that he had marked satyriasis and had been unable to attend to 
his business, thrown about his money, slept badly, rambling round 
the house at night, and for days had taken nothing but beer. 

Physical condition. —Tongue, clean tremulous; palate high; 
right eye blind, left good sight, pupils Argyll-Robertson ; hearing 
good; deep reflexes lost; gait ataxic; fine tremor of hands; marked 
anaesthesia of legs, mostly on right side. Impaired sensibility of 
hands and face, “ padded foot,” girdle pains, has had gastric crises, 
and alcoholic gastritis. 

Mental condition .—Great loss of memory, especially for recent 
events. Restless, and of dirty habits, and full of delusions. A 
little later, March, 1897, he is much distressed in his mind by fixed 
delusions of persecution. “His execution has been ordered, every 
hour is his last, so that he lives in continual dread that they are 
going to fetch him away to hang him. M 

July, 1898.—He is in good bodily health, but there is a recur¬ 
rence of persecutory delusions in another form. “ Lions and tigers 
are after him to devour him, and he begs for protection against 
them,” causing him to be noisy and excited. 

February, 1899.—Patient attacked by dysentery, from which 
he recovered. A later note states that he had swallowed stones 
with suicidal intent. 

Health deteriorated, shows signs of tabes of a mixed type, 
anaesthesia and analgesia of both extremities and trunk, with 
thermal loss and complete loss of muscular sense—slight ptosis 
and paralysis of external rectus of both eyes—Romberg sign present', 
Argyll-Robertson pupils, plantar reflexes almost absent, abdominal 
brisk, knee-jerks absent. 



Mental condition varies from time to time, sometimes much 
more lost, deluded, and incoherent than at others. 

November, 1900.—His physical and mental condition had 
improved considerably. The memory is still bad, especially for 
recent events, but he has now no hallucinations or delusions and 
can talk in a fairly coherent manner and play a good game of 
draughts. He has also some knowledge of chess. There is much 
less ataxy and he does not sway when the eyes are shut. The 
anaesthesia and analgesia are much less and limited to patches on 
the lower extremities. 

August 6, 1900.—Patient is quiet, has absence of all the deep 
reflexes, some hypotonus, no marked ataxy, no tremor in hands, 
can undress and dress himself, standing on one foot to put the other 
through the trouser leg, and able to put on his trousers himself, 
standing, so that there is very little unsteadiness of position. He 
can feel light tactile impressions correctly all over the body with 
the exception of a patch about the size of a crown piece below and 
internal to the left nipple, where he several times did not respond. 
Pricked with a pin even sharply, he says that it feels like the point 
of a lead pencil. When shown that it was a needle he was much 
surprised. Tested with test-tubes of hot and iced water, there was 
considerable delay in responding to the hot water, but he always 
said it was hot. Tested with ice water, he responded quicker and 
said it was hot and burnt him. He never once said it was cold. 
In fact, given to him with his eyes open to grasp in his hand, he 
said it burnt him, and he could not be induced to take it again. 
There is no loss of joint sensation and no loss of sense of position. 
There is well-marked, old optic atrophy of the right eye, some 
impairment of the sense of smell, none of taste. His mental con¬ 
dition indicates considerable dementia, he thinks that it is April, 
he does not know how long he has been here. He can give a 
pretty clear account of his previous life, which must have been a 
dissolute one. 

Case 71.— Tabes , osteo-arthropathy , drink , syphilitic history , hemi¬ 
plegic attack , mania f dementia , mental improvement , pronounced 
signs of tabes. (Reported by W. F. Forshaw, M.R.C.S 

C. W., admitted to Claybury Asylum, July, 1900. Age on 
admission, 41. Occupation, ironer. Married, but has no children ; 
has had no miscarriages. Shortly after admission was diagnosed 
as post-hemiplegic mania. 



Resume of patient's history previous to admission (her own 
account of it).—Had her left arm “ pulled out when a girl/’ Has 
always been subject to ulcerated throats. Hair used to come out 
in combfuls. Barmaid for five years, addicted to drink (beer, 
whisky). Slipped down in street and fractured right tibia. “ She 
was only aware that the leg was broken when she looked down at 
it and saw the bone sticking up.” It was therefore painless, and 
indicated tabetic bone lesion. Had a seizure in street one year 
previous to admission, became unconscious and paralysed on right 
side after it. Attended Brompton for phthisis, and was advised to 
go abroad. 

Mental state on admission (July, 1900).—She was very excitable 
and restless, wished she was dead, said “ she was tired of life.” 
She was dangerous to others, and threatened to kill the workhouse 
officials because they had been making irritating charges against 
her, and because she had been starved and illtreated. She soon, 
however, became depressed and despondent, and could not or 
would not give a rational account of her past life. 

Physical condition on admission .—She was unable to walk, and 
had a right-sided hemiplegia. Her knee-jerks were not obtainable, 
and her pupils did not react to light or accommodation. She had 
no physical disease of the lungs or heart. Her right knee was 
much enlarged and leg everted ; the patella was on the outer side 
of the joint, her foot was at a right angle outwards due to the ill- 
setting of an old fracture of the tibia. She was generally impaired 
in health and bodily condition. 

A fortnight after admission her temperature suddenly rose to 
103*8°, and she was unable to speak. No physical signs of illness 
found in any of the viscera ; three days after this sudden onset of 
fever, she began to have seizures chiefly affecting the right side, 
numbering thirty-one in all. Ten days after cessation of seizures 
she was well again as regarded her speech, &c. She gradually 
improved physically, and two months later she was able to walk. 
She became quieter mentally, though had frequent maniacal out¬ 
breaks, and assisted in the ward work, and has remained in this 
state up to the present time, which will now be described in 

Present condition (March, 1902): Mental .—She is quiet and 
orderly, answers questions directly and correctly, has a good 
memory for remote and recent events, and is very anxious to get 
out of bed to help with the work. Physical .—There are no signs 
of hemiplegia now; her right leg is practically a “ flail leg,” it does 
not touch the ground when she is standing straight, quite two 


inches shorter than the other. This shortening is at the knee 
joint and in the leg itself. The right knee-joint is swollen and full 
of fluid (fluctuation to be had easily, also the patella tap). There 
is great disorganisation, the patella is on the outside of the joint, 
there is a loose body in the joint just above the patella, which feels 
like a piece of bone probably broken off from the external condyle; 
crepitus is to be had easily by rubbing it against the patella; 
the internal condyle of the femur is very much expanded, es¬ 
pecially antero-posteriorly, the joint is much wider than the 
corresponding one. This swelling came on suddenly, and reached 
its present.size in three days ; it is painless, and the skin is not 
abnormally heated. Her foot is more everted than it was on 
admission owing to the condition of the knee, and her leg moves 
abnormally in extension, flexion and rotation. Other joints of 
body appear normal. Her pupils and knee-jerks remain as on 
admission. She had an attack of acute shooting pains through 
the right side of her abdomen three weeks ago, “ like knives 
running into me,” and vomited in consequence. The sensation of 
her legs is very much changed. This change is most marked on 
the left leg, especially in the region supplied by the fifth lumbar 
root; she was anaesthetic to light touch over this region, could 
not discriminate between prick or touch, or hot or cold. Some¬ 
thing similar on right leg, but not so marked; could distinguish 
between hot and cold. Sensations very faulty generally over both 
legs. There is no analgesia of thorax, but there is a well-defined 
belt of trunk light tactile anaesthesia extending from the lower 
border of the third rib to the lower border of the sixth rib, both 
front and back. Heart and lungs appear normal. She has 
had difficulty with her urine lately, and three days ago she had 
to be catheterised, 45 ozs. drawn off. Since then she has passed 
urine regularly, averaging between 60 and 70 ozs. per diem. She 
has a median scar on palate, it looks like an old cleft-palate 
operation. She speaks with a lisp. 

A week later, April 4, 1902.—Patient has been in bed for the 
last ten days. The swelling of the right knee is much less marked; 
there is no heat or redness. General improvement since. 

Interesting Hospital Cases. 

Case 72.— Macropsy and micropsy, transitory aphasia and right 
hemiplegia, doubtful diagnosis of general paralysis or syphilitic 

brain disease. 

H. B., aged 43. Came to Charing Cross Hospital for weak¬ 
ness in the legs. History of syphilis from the doctor. Pupils of 



medium size, sluggish reaction to light. Knee-jerks present both 
sides. After leaving the hospital he was affected with a transitory- 
aphasia and a right hemiplegia. Rigidity in his right arm and 
leg set in and persisted. He did not lose consciousness, but he 
suffered for some time with a headache; later on he was affected 
in the following way : whilst sitting at home he complained to his 
wife that the picture frames were empty, his trousers were moving 
up his legs, and that the handkerchiefs on the table were moving 
towards him. He could not sleep, and said the bed was being 
pulled away from him, and the sheets were being plaited. This 
was the first time his wife noticed anything wrong mentally. On 
April 28, on taking a walk with his wife he suddenly became 
rigid and drawn to his right side, nearly causing him to fall. 
Patient says that two years ago he had tingling sensations in his 
right foot, which he afterwards felt in his left foot. For the last 
six months he has had some difficulty in getting from his bed to 
the floor, having lost sensation in his feet. He has lost three 
stone in weight during the last year. There is nothing else note¬ 
worthy in his past personal history, except for the fact that for 
the past fifteen months, according to his wife, patient has dragged 
his right leg in walking. 

Present condition. —Patient is pale, has a drowsy apathetic 
expression. He answers questions slowly, and although he is 
fairly accurate in his answers, it appears to cause him trouble in 
comprehending what is said, and in recollecting in order to answer. 
Both pupils equal, react sluggishly to light. Discs: nothing 
definitely abnormal discovered by Mr. Collins. Patient says his 
eyesight is becoming worse, and he complains that things appear 
to move, and that objects sometimes appear too large, and some¬ 
times too small. 

Case 73.— One of a family of six suffering with Friedreich's disease. 

Pains, but no loss or diminution of cutaneous sensibility. 

Marked ataxy. 

A. W., aged 37, admitted to St. Pancras Infirmary, October 19, 
1900. She is the eldest of six members of her family, all affected 
with Friedreich’s disease. She was an out-patient under Dr. 
Ormerod for twenty-one years. 

Family history. —On the father’s side there is a history of fits, 
on the mother’s side, grandfather paralysed. The illness began 
when she was 35 with jerky movements which the doctor thought 
was chorea. She was able to walk up to the age of 31, since then 


her speech became affected, her back more curved, and the 
muscular weakness more pronounced. She is very feeble, being 
hardly able to raise the legs from the bed or to sit up, but able to 
use her hands and knit, but she would be unable to do this in the 

Present state .—Patient has a rather weak, fatuous, but mobile 
expression, there is more paresis on the right side of the face than 
on the left, the tongue is protruded slightly to the right. Her 
speech is thick, somewhat indistinct, slurred, lisping, and occa¬ 
sionally stumbling, but she is able to pronounce all the letters, 
and there does not appear to be any more difficulty with one word 
more than another. There is no tremor in the lips or tongue, 
and I could detect no nystagmus, although there were irregular, 
oscillating movements of the neck. The grasp is very feeble, and 
there is a difficulty and a slowness in unclasping the fingers, so 
that the hand seems to stick. She had suffered much with shoot¬ 
ing pains, and they cause her legs to jump a great deal. There is 
marked ataxy and loss of sense of position in the hands, but she 
knows what I am doing when I straighten or bend the fingers, 
showing that she can appreciate joint sensation. In the lower 
limbs there is marked talipes equino varus, the muscles are 
somewhat wasted, the deep reflexes lost, the superficial plantars 
exaggerated. There, is but moderate hypotonus. Sensibility to 
pain and touch good and correct in localisation, but the response 
is slow; but this may be only due to slow mental reaction, which 
is very marked when you converse with her. The epigastric 
reflexes on the left side lost, but slight crossed reflex oi the right; 
right side absent, no crossed reflex. There is no anaesthesia or 
analgesia anywhere in the trunk, there is very marked scoliosis of 
the spine, which is due to a dorso-lateral curvature to the right. 
There is great weakness of the trunk muscles and of the erectores 
spinae. She is quite clean in her habits, careful and intelligent, 
and in good bodily health, save the paralysis. 

Case 74.— Examples of optic atrophy affecting one child , facial 
paralysis another , and several others suffering with fits . No 
signs of syphilis on the body , but a certain history of syphilitic 
infection of the mother. 

This family history is of interest, because, had I not been able 
to obtain full particulars from the practitioner, I could not have 
found either from the mother or the examination of the children, 
that syphilis was the cause of the optic atrophy in the child who 
was brought to see me on account of blindness. 




F. C., aged 11, was brought to me by Dr. Atkin suffering with 
blindness of both eyes since he was 7 years of age. The right eye 
became first affected, and then the left. He attended Moorfields 
for four years without benefit for optic atrophy, cycloplegia, and 
iridoplegia: on the card it is put, (?) Syphilis congenital. There are 
no signs of congenital syphilis now on the body, although Dr. 
Atkin informs me that he treated the boy when an infant for 
snufHes and a rash. Up to nine months ago he could see to play 
with other children, but he has gradually become quite blind, and 
has been sent to a blind school. There is slight evidence Of facial 
paresis of right side, and the tongue protrudes towards the right. 
Grasp is good in both hands, and there is no loss of power. All 
deep reflexes somewhat exaggerated. Mentally he is intelligent, 
quick witted, and comprehends well. 

History of maternity .—Mother married eighteen years, six 
children, and one miscarriage. Such a history with no signs of 
syphilis on the bodies of the children would allow the statement, no 
history of syphilis ; in fact, some authorities would cite this case 
as one, proving that optic atrophy could arise independently of 
syphilis; perhaps it can, but this and many other cases that are 
cited do not prove it. 

Miscarriage, seven months; (1) Boy, died in a fit, aged 1 
year and 9 months; (2) Girl, now healthy, aged 15 ; (3) Girl, now 
healthy, aged 13; (4) Boy, the patient, aged 11, optic atrophy; 
(5) Boy, aged 9, left facial paralysis at six months, commencing 
optic atrophy ; (6) Boy, aged 6, fits until five years old. 

Dr. Atkins informed me that the mother, three months after 
marriage, suffered with sore throat, ulceration of the womb, and a 
characteristic rash for which he treated her. 


Morbid Anatomy and Pathology. 


We have already seen that the clinical cases show all 
grades of tabes with slight mental symptoms and pro¬ 
nounced cord symptoms to those of very pronounced mental 
symptoms and slight cord symptoms. Consequently there 
must be a number of intermediate cases between the two 
extremes, and it would be extremely difficult to decide 
whether they should be called tabes or general paralysis, 
and the invention of the term tabo-paralysis is an indication 
of this clinical difficulty. In like manner, and as a matter 
of expediency (especially among private patients) such cases 
are at first called locomotor ataxy. There can be no hard 
and fast clinical line between the two diseases ; etiologically 
I have shown that they are practically identical; are they 
pathologically so ? This question can be studied best by an 
examination of a sufficient number of these intermediate 
cases. Nageotte asserts that he found changes in the 
posterior columns in two-thirds of all forms of cases of 
general paralysis, and he looks upon the diseases as patho¬ 
logically identical. Fiirstner, who has made a most careful 
study of this subject, does not agree with Nageotte that the 
spinal cord exhibits typical tabic lesions in anything like so 
large a proportion. He concludes that the spinal cord is 
invariably affected in some part of its structure in general 
paralysis; he states that there certainly occur cases where 
the spinal lesion is first; also a series of clinical symptoms 
corresponding with the anatomical findings. 

Dr. Watson finds posterior column degeneration of 
exogenous systems in five out of eight cases of juvenile 
general paralysis. 

If it be admitted that syphilis is the most important (if 
not essential) cause of both these two diseases, and very 
strong proofs now exist of the truth of this doctrine, which 
is daily becoming more widely accepted, then, just as we 
find that alcohol, lead, diseased maize, ergot, and other 



poisons may produce in one individual a morbid process in 
the brain, cord or peripheral nerves, while the disease pro¬ 
cess attacking the nervous system is essentially the same, 
so I will endeavour to show that the effect of the syphilitic 
poison on the nervous system may in one person produce a 
degeneration of the spinal afferent protoneurons, in another 
of the optic nerves, or the cerebral cortex, and, according 
to the structure affected primarily, the disease is classified 
as spinal tabes, optic tabes, tabo-paralysis or general 

Here I will also take the opportunity of remarking that 
some of the most rapidly progressive cases of paralytic 
dementia have been those in which, simultaneously with 
the brain affection, there has been cord affection also. A 
case of juvenile paralysis, published in the first volume of 
the Archives of Neurology, p. 278, died within four months 
of the onset of the disease; several other cases (68, 69) 
likewise show a rapid progress. The onset of the cerebral 
symptoms generally, but not necessarily, leads to a cessa¬ 
tion of the morbid process affecting the spinal cord and 
vice versa ; it may then be asked, is the disease one affect¬ 
ing the vital energy of the neurons of the whole nervous 
system ; and in the struggle for existence, do those die 
upon which the greatest amount of stress falls, aided by 
contributory precarious vascular supply, or some devitalis¬ 
ing condition, especially hereditary defective durability? 
How can, however, the environment affect the decay of 
structure, unless there is a deficiency in the nutritive pro¬ 
perties of the environment of the neurons ? 

We might assume, hypothetically, that there is some bio¬ 
chemical defect or subminimal deficiency in the blood, the 
lymph, or the cerebro-spinal fluid, by which nervous meta¬ 
bolism may be rendered incomplete. Those nerve structures 
with the highest vitality, in a struggle for existence, would be 
able thus to extract a sufficiency of the necessary complex 
phosphorised materials for maintaining physiological equili¬ 
brium and for the formation of protagon ; whereas, if there is 
a total insufficiency, those with less vis propria would first 
waste and undergo atrophy. A vicious circle is very apt to 


be established when structures presiding over important 
functions of the body are diseased, and then secondary com¬ 
plications arise and may be mistaken for the initial cause. 
I look upon these diseases as primarily a premature process 
of decay ; the term “ abiotrophy ” recently introduced by Sir 
William Gowers {Lancet, May, 1902) expresses aptly in one 
word what has been said above, and previously expressed in 
my Croonian Lectures. 

The disease, whether it is elective (affecting only some 
particular system of afferent fibres in the spinal cord or the 
optic nerves), or whether it affects only the cerebral cortex, 
is a veritable tabes or wasting. This wasting, however, may 
be general and affect the whole central and peripheral 
nervous systems. In many cases of tabo-paralysis the cord 
is so wasted that in a big muscular man, e.g., Br—, 54, and 
Case 31, the cord was not so large as that of a two-year-old 
child. Both gray and white matter were atrophied, and 
without any proportional overgrowth of glia or thickening of 
membranes. The process as thus seen appears to be a bio¬ 
chemical failure on the part of the neurons to maintain 
physiological metabolic equilibrium. 

The paroxysmal attacks of pains and crises, maniacal 
and epileptiform seizures, are clinical expressions of an 
irritant action, and suggest the formation or accumulation in 
the blood or lymph of some toxin which has a local action, 
unless we assume that the decay of the neurons (terminating 
in death) is accompanied by increased irritability. In the 
discussion of the changes in the brain, we shall see that 
there is much more reason to suspect the existence of an 
irritant toxin which produces acute destruction of the 
neurons and formative proliferation in the vessel walls and 
perivascular lymphathic sheaths, also active glia proliferation 
—all being the results of a conspiracy of morphological 
and biochemical factors. In the case of the spinal cord, the 
thickening of membranes and the changes in vessel walls are 
inconstant, and can in no way account for the elective 
destruction of fibres in the posterior columns; although as I 
have previously said, initial affection of certain segments of 
the spinal cord, as shown by the symptoms—especially the 



cutaneous sensory disturbances—may be explained by a 
precarious vascular supply in these regions; but then, this is 
not the essential factor, only the contributory one. Morbid 
anatomy and clinical observation show that there is both 
systemic and segmental election in the pathological process. 

Methods of Observation. 

The tissues were obtained in a fresh condition and 
hardened in a manner suitable for staining by Nissl, Pal, 
Weigert, Marchi, and Marchi-Pal methods. Various other 
methods were employed (when necessary), such as the 
Heidenhain, Gudden carmine, and Bolton’s iron alum; the 
sections were either cut in paraffin by the large Cambridge 
rocking microtome for the Nissl and Heidenhain methods 
and always of uniform thickness; or, for the other methods, 
cut in celloidin after hardening in Muller or Formol-Miiller. 
A systematic examination was generally made of the spinal 
cord and roots at every level, together with the cauda equina. 
A number of the posterior spinal ganglia were also examined. 
Sections of the brain cortex in various situations, usually of 
Broca, first frontal, ascending frontal and ascending parietal, 
prefrontal, occipital, temporal and angular were made in a 
number of cases by Nissl method as well as by one of the 
before-mentioned methods to demonstrate the fibres. The 
medulla and, in a few instances, the pons and internal 
capsule were also examined; likewise the optic nerves and 
in some instances the retina, the peripheral nerves of the 
skin and muscles in a few instances, and in a considerable 
number of cases, the ulnar, median and sciatic nerves. I do 
not lay claim to have examined all these tissues in so 
systematic a manner as I have the cord and cerebral cortex; 
the observations have been made rather with a view of 
establishing the fact that the disease is one primarily of the 
central nervous system, and that the peripheral structures 
are affected later in the disease. 

The. spinal cord lesions of tabes and tabo-paralysis as 
regards the affection of the posterior roots and posterior 
columns are, as a rule, identical. In both diseases there is 
the same system of exogenous fibres affected in the same 


situations in the spinal cord. The morbid process elects 
first certain groups of fibres and spares others, but even¬ 
tually, in advanced cases, destroys nearly all the exogenous 
fibres. Many symptoms and signs, and especially the distri¬ 
bution of anaesthesia in the case's of tabes and tabo-paralysis 
(in which the cutaneous sensibility could be ascertained), 
indicated that certain segmental regions of the spinal cord 
are earliest affected; and systematic microscopic examina¬ 
tion of the spinal roots and of the spinal segments showed 
that certain regions are more affected than others—viz., 
lower lumbar and sacral, mid, upper dorsal and lowest cervi¬ 
cal. With few exceptions all the spinal cords were obtained 
from well-defined tabo-paralytic cases; but in some of those 
dying within the last year, I have systematically examined 
the patients for cutaneous anaesthesia, and made charts of 
the same, and correlated the results (Cases 3i and 46) with 
the microscopic investigation. Charts of the spinal degen¬ 
eration at various levels have been made by means of 
Edinger’s projection apparatus, so that the distribution of 
the degeneration can be studied at a glance. 

Posterior roots .—Sections of the cauda equina in most of 
the cases were made by tying all the roots together, and 
embedding in celloidin. Microscopic examination almost 
invariably showed (whether the case was early or late) that 
degeneration or disappearance of fibres had taken place, 
relatively proportional to the atrophy of the exogenous system, 
in the lumbo-sacral region of the cord. Sections, longitudinal 
and transverse, which had been stained by Marchi fluid very 
seldom showed any degenerated black fibres, and they pre¬ 
sented none of the appearances of Wallerian degeneration of 
nerves. When stained by Pal or Weigert, some fibres which 
stained blue might be normal in appearance, others appeared 
very much attenuated, as if the myelin sheath had atrophied; 
moreover, they stained a fainter blue owing to the thinning 
of the myelin. The bundles of posterior roots, which are 
normally considerably larger than the anterior roots, were 
much smaller and diminished in size, in proportion to the 
outfall of fibres. The interstitial tissue was sometimes in¬ 
creased, although there was not always a proliferation; the 



vessels were often seen engorged with blood, but not more so 
than those of the undegenerated anterior roots. The walls of 
the arteries and arterioles were more often normal than not; 
when thickened, it was generally in a subject over 50, and 
the thickening was not limited to the posterior roots, but 
affected also the arteries of the comparatively healthy 
anterior roots. I do not remember seeing one which pre¬ 
sented the typical character of recent syphilitic arteritis, 
though it is not uncommon to find a condition of arterio¬ 
sclerosis, which might, of course, be indirectly of syphilitic 

Teased preparations of the posterior roots were made 
and stained with Marchi, with logwood and ammonium 
picrate, and with various other stains. The appearance pre¬ 
sented reminded me of the condition found in a nerve after 
section, when all the products of degeneration have been 
absorbed. Empty neurilemmal sheaths with proliferated 
nuclei, vessels and connective tissue are the only structures 
found, as a rule, in the roots which have undergone degen¬ 
erative atrophy. Some fibres still possessing a myelin sheath 
may be found amidst this tissue, if the root-fibres are not 
completely destroyed (vide fig. 38). The myelin does not 
show black globules like a degenerated nerve-fibre, but occa¬ 
sionally a fine black dust scattered through its substance, as 
if a slow molecular Wallerian change was taking place; or 
the myelin might be simply diminished in amount, and 
attenuated to various degrees in some places, while of fair 
thickness in others. Where the myelin is diminished, 
several nuclei of the neurilemmal sheath could be seen, as 
if the atrophy of the myelin had been followed by, or asso¬ 
ciated with, nuclear proliferation. Phagocytes containing 
blackened myelin were seldom seen, except in some few 
cases of rapid tabo-paralysis. 

The roots in a case of ataxic paraplegia, where there was 
marked degeneration of all the long tracts of the spinal cord, 
presented quite a different appearance; for the myelin 
sheath was of normal thickness, showed nodes of Ranvier, 
and a very little interstitial tissue, and only the normal 
number of nuclei in the neurilemma. Some of the fibres 


showed an appearance like Wallerian degeneration, but the 
majority showed no change; the morbid process was there¬ 
fore intraspinal, whereas the degeneration of the sensory 
posterior spinal neurons of tabes is intradural, for the degen- 

Fig. 38. 

Two fibres from posterior root, eleventh dorsal, Case 49. Magnifica¬ 
tion, 400. 

erative atrophy extends back as far as the spinal ganglion. 
My results, therefore, conform in great measure to the 
observations of Philippe upon this point. Before dealing 
more in detail with the distribution of the intraspinal degen- 



eration of the exogenous system of the posterior columns, 
and the additional degeneration of other systems which may 
occur, we shall consider the changes which may be observed 
in the spinal ganglion itself. 

Spinal ganglia .—The attractive theory of Marie based 
upon the neuron doctrine that the degeneration is due to 
a nutritional change in the posterior spinal ganglion cells is 
one which explains many facts, but the argument which 
is advanced against it is this: if it be so, why are not 
nutritional changes manifested histochemically by the Nissl 
method ? Some authorities, Wollenberg, Strobe, and others, 
have described changes in the posterior spinal ganglion 
cells; on the other hand, numerous observers have asserted 
that the changes which have been found were insufficient 
to account for the changes in the roots and cord. The 
examination of a large number of sections of posterior 
spinal ganglia, from the majority of the fatal cases I have 
recorded, has not satisfied me that the changes which I 
observed were sufficient to account for the disease. The 
changes in the cells were indeed insignificant as compared 
with the degenerative atrophy of the fibres emerging from 
the ganglion. In many instances, some few of the cells 
were shrunken, the nucleus eccentric and even the capsules 
empty, as if there had been a complete atrophic decay ; but 
the majority appeared fairly normal, both the large, medium, 
and small sized. Frequently excess of pigment was seen, 
but the same might be found in the cells from any old person. 
Sometimes the great majority of cells of a ganglion stained 
blue by Pal, and by examination with an oil immersion, it 
was found that the protoplasm was beset throughout with 
fine dust like blue particles. The same may be seen in 
early fatty degeneration of muscle when stained by this 
method, and it may be that the protoplasm of the cells have 
undergone a recent fatty degenerative change. Stained 
with Marchi the same cells for the same reason may appear 
black. The process to my mind is acute, and may well be 
due to complications occurring in the tabo-paralytic towards 
the end of life. 

Sections of posterior roots in animals did not, I find. 


give rise to any degeneration of the spinal ganglion cells. 
Lenhossek at first thought there was a change, but fur¬ 
ther observations caused him to renounce this opinion. If 
neurilemmal cells play an important part in tabes, why 
are posterior roots invariably degenerated back to the 
ganglion ? 

Peripheral nerves—white rami, gray rami, sympathetic .— 
In a number of cases the peripheral nerves were examined, 
median, ulnar, and sciatic, sometimes the nerves of the 
skin, sometimes the nerves entering the muscles, e.g ,, 
vastus interims. The white rami, gray rami, and sympathetic 
were also examined in a few cases, but a more systematic 
examination is now' being carried on by Dr. Goldschmidt. 

It may be stated generally that the peripheral cerebro¬ 
spinal nerves like the spinal cord of advanced cases of 
tabo-paralysis were smaller in trans-section than normal, 
and without any microscopic examination it would be said 
that they were apparently atrophied. 

A section longitudinally through the spinal ganglion with 
a portion of the roots and issuing nerve attached stained by 
Weigert method, and examined microscopically, leaves no 
doubt in the mind of the observer that the disease is essen- 
. tially one of the intradural portion of the spinal afferent 
neuron. He will observe the anterior root, consisting of 
normal fibres, lying by the side of the degenerated and 
completely atrophied posterior root (fig. 39), and he will con¬ 
clude that no mechanical process of strangulation at the 
point of exit from the dural sheath will explain this fact. 
At the proximal end of the ganglion he will see very few 
fibres, and these much attenuated; whereas, at the distal 
end he will observe the fibres emerging of normal appear¬ 
ance, and as well stained as the fibres of the anterior roots. 
Again, he will consider that it is impossible for a vascular 
change within the ganglion to account for the distal portions 
of the T-shaped processes of the cells to have escaped. 

I have, however, noticed in longitudinal sections of the 
posterior spinal ganglion with a long attachment of the 
ventral and dorsal roots, that the myelin sheath of fibres, 
which still possess the property of staining blue by the Pal 



or Weigert staining, becomes sometimes more attenuated 
and fainter as one proceeds away from the ganglion 
towards the cord. Again, one may find the peripheral fibres 
proceeding from the ganglion quite healthy in appearance 
(as regards myelin staining) in an advanced case of tabes, 
and yet the remote sensory fibres degenerated. Dr. Anderson 
has kindly allowed me to quote some valuable observations 
which he has made upon the development of the myelin 
sheath in the posterior roots and peripheral nerves bearing 
upon this point, to be described later. 

Pig. 39. 

Photomicrograph of a transverse section of the posterior root (third lumbar). 
The small, dark round bundle of fibres is the undegenerated anterior root, the 
large sclerosed root is the posterior. Section stained by Weigert hrematoxylin. 
Magnification, 20. 

Examination of the Peripheral Nerves. 

Transverse and longitudinal sections in some advanced 
cases showed changes, but in no degree sufficient to account 
for the symptoms, or in any way proportional to the atrophy 
of the posterior roots. The ulnar nerves of Case 31 showed 




recent degenerative changes; some of the fasciculi of fibres 
contained a few black stained fibres by the Marchi method, 
due, apparently, to Wallerian degeneration; and in some 
places there seemed to be an excess of interstitial tissue and 
a diminution of fibres. In Case 49, however, where there 
was extensive muscular wasting of the small muscles of the 
hands with reaction of degeneration, and atrophy of the 
anterior horn cells and anterior roots, there was naked-eye 
degenerative sclerosis of the median and ulnar nerves. 
This was quite apparent when the nerves (after hardening 
in Muller) were cut in transverse sections, and showed a 
marked atrophy of fibres with substitution fibrosis. The 
sciatic nerve likewise showed a similar change; but there 
was not the same atrophy of the anterior horn cells, as seen 
in the cervico-dorsal region; the cells in the lumbo-sacral 
region, on one side more than the other, showed a process of 
regressive atrophy; the cells were there, but their processes 
were broken off, and there was not the same degeneration 
of the anterior roots. The process was very probably the 
same, but not so advanced, as in the cervico-dorsal region; 
still the outlying portions of the neurons had undergone 

The cause of this degenerative atrophy will be further 
discussed later; also, considerations will be advanced as to 
why the central projections of the posterior spinal neurons 
should be degenerated when the distal remain unaffected ; it 
is generally admitted that the peripheral terminations of the 
nerves in skin and muscles are more likely to show degen¬ 
erative atrophy than the portions nearer the cells of origin. 
My examinations of the skin are not sufficiently numerous, 
nor do I think the methods usually employed are sufficiently 
reliable, to make any definite statements with regard to the 
importance of the changes; yet the examinations I have 
made were sufficient to convince me that in early cases 
there was little or no appreciable degeneration, while in the 
late cases, although there was undoubtedly atrophy and dis¬ 
appearance of fibres, the changes were of far less importance 
as compared with changes in the posterior roots. This coin¬ 
cides with the obvious segmental root distribution of sensory 
disturbances observed during life. 



The white rami were examined in a few cases in serial 
section; it was observed that there were some large 
medullated fibres, which could be traced into the sympathetic 
trunk, and a large number of small medullated fibres, together 
with some gray sympathetic fibres. 

The Exogenous Systems of the Posterior Columns. 

In all the twenty-eight cases examined, the three sets of 
coarse fibres entering the cornu-radicular zone, and proceed¬ 
ing respectively to the root zone of Charcot, to the cells of 
Clarke’s column, and to form Goll’s column, were affected; 
not always, however, to the same extent, for the relative 
degree of degeneration of each of these three systems of 
fibres depends upon the relative degree of degeneration of 
particular roots. For, although every root in the lumbo¬ 
sacral region, where the morbid process in the great 
majority of cases commences, contains fibres belonging 
to each of the three systems, namely, spinal, cerebellar, 
and cerebral, yet some roots, according to the functions 
of the structures innervated by them, contain many more 
cerebral afferent fibres than cerebellar and vice versa. The 
appearance of Clarke’s column at the level of the second 
lumbar segment and its disappearance at the second dorsal is 
an indication of the important relation of this system of 
neurons to the muscles of the trunk and the muscles used 
in maintaining the static position. 

I have shown 1 experimentally that the very large first 
sacral posterior root of the monkey possesses a large num¬ 
ber of fibres belonging to all three systems, but especially to 
the cerebral system ; this root is distributed to the whole of 
the sole of the foot and its deep structures ; it is, therefore, 
of great importance in conveying sensory impulses essential 
for the maintainance of gait and station. 

Examination by the Marchi method of the different 
segments of the cord, after section of this posterior root 
in the monkey on one side, showed: (1) That a very large 

number of fibres of this root enter into the formation of the 

■ “ Die Zufulirenden Kleinhirn Bahnen des Ruckenmarks bei den Affen.” 
F. W. Mott. Monatsclvrift fur Psychiatric , vol. i. 


column of Goll, apparently nearly half of the fibres of this 
tract in the cervical region being degenerated, and the 
degeneration uniformly distributed over the whole triangle ; 
{2) that a considerable number of fibres enter the root zone 
of Charcot, in the first sacral segment especially, but also in 
the segments above and below; (3) that at the third lumbar 
segment the only degenerated fibres found in the posterior 
column consist of a band which extends from the mid line 
back to the periphery, leaving internal to it a small triangle 
undegenerated, probably tail fibres. 

Fig. 40. 

Photomicrograph of section (third to fourth lumbar segment) of spinal 
•cord of monkey, after section of first sacral on one side. The black band 
seen represents the degenerated fibres belonging to the cerebellar and cerebral 
systems. It will be observed how very extensive this degeneration is. As 
soon as Clarke’s column appears at the first lumbar a'large number of these 
black fibres run forward to end in a plexus around the cells, leaving the fibres 
of Goll’s column as a compact triangle posteriorly. 

As soon as Clarke’s column begins to appear at the upper 
part of the second lumbar segment, the anterior half of 
these degenerated fibres runs forward to end around its cells; 
and not until about the eleventh dorsal segment do these 
degenerated fibres cease to be found entering Clarke’s 
column. The degenerated fibres of Goll’s column then form 
a definite posterior internal triangle, which can be followed 
up to the medulla. This experimental evidence shows what 



a very important part this root, which is so often affected 
in tabes, must play in the production of ataxy of gait and 
station, by the cutting off of guiding sensations to the 
cerebrum and cerebellum. 1 

The padded foot or complete anaesthesia of the sole, with 
abolition of cutaneous reflex, means, therefore, abolition of 
the fibres for cerebral and cerebellar impulses, and explains 
the increase of the ataxy when the sole of the foot is 
anaesthetised by cold. The ataxy, I am of the opinion, has 
a decided relationship to the atrophy of the plexus around 
the cells of Clarke’s column, and I have not seen any case 
in which this was pronounced without marked ataxy, 
whereas I have seen other examples in which this was 
not pronounced, although Goll’s column was markedly 
affected. Several cases showed comparatively little cuta¬ 
neous anaesthesia, and yet there was very marked ataxy. 

There is another set of exogenous fibres which, according 
to Bechterew, convey sensations from the skin ; these fibres 
are small in size and run a very short intramedullary course. 
In the lumbo-sacral region they occupy at least two-thirds 
of the zone of entry, or zone of Lissauer, and give origin 
to numbers of fine collaterals which arborise around the 
cells of the posterior horn. They do not, therefore, take part 
in the formation of the posterior column, and it may be 
presumed that these fibres convey sensory impressions from 
the skin. This is more easy to understand if we accept the 
hypothesis that the same fibres conduct pressure and pain 
impressions, but that quality and intensity of stimulus 
determine the sens’ation produced. In syringomyelia, how¬ 
ever, we have sensory dissociation, touch being perceivable, 
but heat, cold, and pain not, for the reason that the 
grey matter is destroyed and the exogenous fibres of the 
posterior column are intact; it may be presumed then, that 
the gray matter conducts painful sensations, and the posterior 
columns conduct tactile; but the segments of gray matter of 
the posterior horn are united by long and short ascending 

1 Anderson has found that section of the seventh post-thoracic root (cor¬ 
responding to the first sacral) produces in kittens an atrophy of the cells of 
Clarke’s column, and he confirms the above observations of mine. 


and descending association fibres, and their preservation, 
at any rate for a considerable time, may account for the 
delay, yet eventual transmission of sensory stimuli, in tabes, 
to the brain. 

The fine fibres of Lissauer’s tracts were in a few cases 
not affected at all. In many cases (eleven out of twenty- 
eight) when there was a marked affection of the root zone 
of Charcot, the fine fibres of Lissauer’s tract were but 
slightly affected. In a few instances where it had been 
possible to investigate the sensory cutaneous disturbances 
during life, it was found that there was a relationship 
between the degree and extent of the same, and the degree 
and extent of distribution of atrophy of Lissauer’s tract. 
Head and Campbell call attention to the great number of 
small cells in spinal ganglia of the trunk region as compared 
with the cervical and lumbo-sacral regions. They consider 
that the small cells subserve the function of pain, but some 
are no doubt afferent splanchnic neurons. 

Several fatal cases were examined in which the sensory 
disturbances were either absent or comparatively slight, 
yet the motor incoordination was marked and the previously 
mentioned three sets of fibres in these cases were atrophied. 

Occasionally, as Eedlich and others have observed, in 
early cases terminating fatally acute changes may be found 
affecting the intramedullary portion of the exogenous 
neurons, and.not the roots. Case 52 was an example of this, 
where the patient did not long survive the onset of the spinal 
symptoms, and we find a number of recent degenerated 
intramedullary fibres in the lumbo-sacral region, limited to 
definite systems (fig. 41). The coarse internal fibres entering 
the cornu radicular zone are seen degenerated at all levels of 
the lumbar and sacral regions; the black degeneration pro¬ 
ducts are neither found in the entering zone of fine fibres of 
Lissauer’s tract, nor in any of the sections of the posterior 
roots attached to the sections of the cord; the degeneration 
is therefore intramedullary and selective. 

No cutaneous disturbance was observed during life, al¬ 
though there was ataxy; the coarse degenerated fibres 
belonged to (1) spinal reflex, (2) cerebellar, (3) cerebral 




afferent systems, and occupied respectively (1) the root zone, 
terminating at the base of the posterior horn, (2) the fibres 
entering Clarke’s column, (3) the fibres entering Goll’s 

There was no meningitis which could account for this 
intramedullary degeneration; moreover, if this were the 
cause, it should not be selective in sparing the fine fibres of 
Lissauer’s tract. In such a chronic disease as tabes usually 
is, it is quite probable that a process of degeneration akin to 

Fig. 41. 

Section of spinal cord, first lumbar, Case 52, showing degenerated fibres 
in the cornu-radicular zone, C.R. The posterior roots are free from degenera¬ 
tion ; so is Lissauer’s tract. 

Wallerian degeneration frequently occurs, the products being 
absorbed; but it is likely that all degrees of the process of 
myelin disintegration may take place; in some instances 
it is slow wasting, due to disintegration exceeding normal 
integration, and involving a gradual process of atrophy; in 
other instances, a rapid acute disintegration occurs akin to 
Wallerian degeneration, and between the two extremes there 
are probably all grades of destructive change. 



The Endogenous Systems of Fibres of the Posterior Columns. 

In the nine cases where there were very marked ataxic 
symptoms, the following results were obtained by micros¬ 
copical examinations :— 

(1) The descending endogenous system of fibres was 
markedly affected in six instances, and in three very markedly. 

(2) The ascending endogenous system (cornu-commissural 
of Westphal) was never completely destroyed throughout the 
cord, even in the most advanced cases, although in one or 
two instances, e.g., 49 and another case, notes of "which are 
not recorded, but which is contained in the Table, it was 
almost absent in some regions. 

In cases of endogenous system degeneration, there was 
invariably a very marked atrophy of the exogenous system. 
In nearly all the cases which commenced with optic atrophy, 
eventually terminating in blindness, there was no appreciable 
affection of the endogenous system; this, however, was not 
invariably the case, striking exceptions being Cases 28 and 
49. There was a decided relationship between the degree of 
affection of the endogenous systems of the posterior columns 
and the degree of ataxy, moderate atrophy of the endo¬ 
genous systems occurring in persons who were well on in 
the second stage of locomotor ataxy. All those with marked 
or very marked atrophy were in the advanced bed-ridden 
paralytic stage, and one or two presented muscular atrophy. 
All those in the pre-ataxic stage showed no degeneration of 
the endogenous systems, although there was extensive 
atrophy of root-fibres and their intramedullary projections 
in many instances. 

Origin of the fibres of the endogenous systems of the 
posterior columns. —Many observers have shown that trans¬ 
verse lesions of the spinal cord produce descending degenera¬ 
tion of the posterior columns. Dejerine and Theohari point 
out in their communication that Schultz, Bruns, v. Len- 
hossek and Obersteiner consider that the comma tract is 
composed of exogenous fibres; Tooth, Pierre Marie, Gom- 
bault, and Philippe and Daxenberger, that it is composed of 
endogenous fibres. Dufour and Philippe (in his thesis) 



think that the comma tract and the dorso-median degenera¬ 
tion in the lumbo-sacral region represent one and the same 
system of endogenous fibres. Purves Stuart in Brain 
has recently expressed the same opinion, based upon the 
examination of the descending degeneration resulting from 
a crush of the cervical region. Flatau, on the contrary, 
believes that for the greater part of its extent, the descend¬ 
ing degeneration is of radicular origin. Hoche remarks that 
the long extent of the comma tract does not agree with what 
is known of the descending branch of the posterior roots; he 
regards the peripheral degenerated field and the comma 
tract as two independent systems. Dejerine and Theohari 
formulate the following conclusions, based upon an analysis 
of experiments upon animals, and upon the descending 
degenerations observed in the posterior columns in man, in 
consequence of pure radicular lesions, and upon a compari¬ 
son of these degenerations with the descending degenerations 
observed in two cases of transverse lesions of the cord:— 

(1) The degeneration in the comma tract of Schultze is 
due in part to the lesion of the descending branches of the 
posterior roots ; the longest fibres of this tract, however, are 
of endogenous origin. 

(2) The small anterior degenerated zone, which does not 
extend below the segment subjacent to the transverse lesion, 
represents short endogenous longitudinal commissural fibres. 

(3) The peripheral bundle of Hoche, dorsal region (septo¬ 
marginal, Bruce) is continuous with the central oval area of 
Flechsig and the triangle of Gombault and Philippe, and 
represents a very long system of longitudinal commissural 
fibres ; it is a system of endogenous fibres. 

(4) The triangle of Gombault and Philippe contains 
(besides endogenous fibres) a great number of radicular 
fibres ; it is therefore of mixed origin. 

My own observations, experimental and otherwise, tend 
to support these views in great measure, although I am 
inclined to agree with Dufour, Philippe, and Purves Stuart 
that the descending fibres of endogenous origin belong to one 

I consider that these fibres, like the exogenous systems 



of fibres, are of long, medium, and short lengths, and serve 
for the correlation of sensory function of different segments 
of the spinal cord. 

Observation of many cords, in some of which, in the mid 
and upper dorsal regions, there was a complete atrophy of 
the root-fibres in cases where during life there was a corre¬ 
sponding loss of cutaneous sensibility of the trunk, showed 

Fig. 42. 

Photomicrograph, lumbo-sacral region, of an advanced case of ataxy (tabo- 
paralysis). The posterior columns are almost completely denuded of fibres, 
a few are left in the cornu-commissural tract and the oval area of Flechsig. 
There is also sclerosis in the crossed pyramidal tracts on both sides. There 
is not much shrinking of the posterior columns, and the meninges are not 
more thickened posteriorly than anteriorly. The central canal is dilated and 
filled up with glia tissue. 

still a large number of fibres in the situation of the comma 
tract, and the posterior internal zone extending thence along 
the dorsal margin of the posterior columns, and continuous at 
the first lumbar with a small triangle at the side of the 
median fissure. The fibres in this triangle, as one proceeds 
to lower levels, are seen to extend up the median fissure, 



and become continuous with the oval area of Flechsig 
in the lower lumbar and upper sacral regions, and this 
again is continuous with the median triangle of Philippe, 
situated in the lowest sacral segments, vide photomicro¬ 
graphs 42, 43, 44. 

Fig. 43. 

Photomicrograph of first lumbar segment (Case 31), showing cornu-com¬ 
missural zone and posteriorly a small triangle of fibres in the mid-line of 
endogenous origin. 

Fig. 44. 

Photomicrograph of third lumbar segment (Case 52), showing degeneration 
of intraspinal portion of exogenous fibres of posterior columns; the ascend¬ 
ing and descending endogenous fibres are intact. The continuity of the 
fibres of the posterior internal zone, the septo-marginal, and the oval area^of 
Flechsig as one tract, is well shown. 

In cases of apparently complete degeneration of the root- 
fibres in the mid-dorsal region, one finds a set of fibres 
giving off collaterals running on the inside as well as on the 
outside of the column of Clarke: (a) The inner set of fibres, 
continuous partly with fibres of the cornu-commissural zone 
of the same side, partly with fibres of the cornu-commissural 


zone of the opposite side. ( b ) The outer set of fibres coining 
from the posterior horn and running forward to the base of 
the anterior horn, commingling there with the inner set. 

This arrangement is especially well seen in Cases 39 and 
46 ( vide photomicrographs, p. 157 and Plate IV.). 

Cajal has described cells in the middle of the posterior 
horn which give off fibres entering the posterior columns; 
these give rise to ascending endogenous systems of fibres in 
the cornu-commissural tracts, many of the fibres decussating 
to form the posterior commissure. The cells which give 
origin to the fibres of the descending system are possibly 
situated at the junction of the anterior and posterior horns. 

In cases of complete root atrophy occurring in the 
lumbo-sacral, upper, and mid-dorsal regions as exhibited in 
Cases 39, 40, 45 and 49, numbers of very fine myelinated 
fibres can be seen in the substantia gelatinosa of the caput 
cornu posterioris; they can be seen when the fine fibres of 
Lissauer’s tract are completely absent, they form a delicate 
plexus, and can be observed running horizontally across the 
base of the caput cornu posterioris. These are probably 
axis cylinders of the small sensory cells of this region. 
Again, in such cases of absence of root-fibres, numbers of 
fine collaterals can be seen in the gray matter opposite the 
root zone; it is probable that these are derived from the 
descending endogenous fibres. 

In degenerative atrophy affecting the descending endo¬ 
genous fibres the first to disappear are those in the dorsal 
region, occupying the comma-shaped tract, its dorsal club- 
shaped projection and peripheral extension towards the 
median septum; the next are the fibres of the oval area and 
posterior triangle of Philippe, with which they are continuous. 

Degeneration of the Spinal Cord, other than the Exogenous 
and Endogenous Systems of the Posterior Columns in 
Tabo-Paralysis and Tabes. 

In advanced cases of tabes sometimes there may be 
degeneration of the cells of Clarke’s column, and as a result 
thereof, atrophy and sclerosis in the two afferent systems of 
fibres proceeding from these cells to the cerebellum, form- 



ing respectively the ventral and dorsal cerebellar tracts 
(Case 40). 

By far the most frequent and important associated degen¬ 
eration and subsequent sclerosis is to be found in the 
pyramidal systems of fibres. In twenty out of twenty-eight 
asylum cases which I have examined there has been some 
degeneration in some part of the course of the pyramidal 
systems. This pyramidal degeneration is evidence of cor¬ 
tical affection, and is due either to chronic atrophic changes 
in' the cortical psycho-motor neurons or acute destructive 
changes. Sometimes the two are associated. 

Examination of the spinal cords of twenty-eight cases of 
tabo-paralysis has shown me that the affection of the pyra¬ 
midal systems is in relative order of frequency as follows :— 
(1) Primary degenerations. — (a) Primary degeneration of 
both crossed pyramidal tracts, fairly equal on the two sides. 
(b) Degeneration of both pyramidal tracts, but more marked 
on one side than the other ; this degeneration is slow in 
progress, not revealed as a rule by the Marchi method, but 
is shown by those methods which demonstrate sclerosis. 
Sclerosis is only revealed distinctly in the lumbo-sacral 
region in a situation corresponding with the position of the 
crossed pyramidal tract in that region ; it can be followed as 
high as the mid-dorsal region in some cases, but becomes less 
and less discernible the higher we proceed in the cord. Such 
may be partly due to intermingling with healthy fibres, but 
I believe it is mainly due to the fact that this degeneration, 
which does not involve the direct pyramidal tracts, is oc¬ 
casioned by a slow progressive atrophic process affecting the 
cortical psycho-motor neurons with the longest axons, there¬ 
fore those which have their terminal arborisations in the 
lowest regions of the spinal cord. The pyramidal fibres of 
the direct tract have a shorter course and consequently are 
not so remote from their seat of nutrition; as a rule, there¬ 
fore, are not wasted. 

Acute degeneration. — (a) Degeneration of the crossed 
pyramidal tract on one side, and direct on the other. 1 

1 Starlinger has described two cases in which there was degeneration of 
the whole pyramidal tract from the cortex. The same was found by Boedeker 
and Juliusberger, Neurol. Gentralblatt , No. 17, 1897. 


Examined by the Marchi method one usually finds well- 
marked Wallerian degeneration, which may be traced up 
through the medulla, pons and capsule to the cortex, and is 
due to destructive changes in the cerebral cortex of one hemi¬ 
sphere ; it is associated clinically with unilateral epileptiform 
seizures and hemiparesis or hemiplegia; sometimes with 
hemianaesthesia and hemianopsy, Cases 45, 54. ( b) Bilateral, 
but usually unequal, degeneration of both crossed and both 
direct pyramidal tracts, which can he traced up to the cortex, 
associated clinically with severe bilateral epileptiform con¬ 
vulsions, and sometimes opisthotonus or emprosthotonus. 
The acute vascular changes in the cerebral cortex may be 
due to arterial thrombosis, brought about by syphilitic 
endarteritis, causing localised and general softening; this, 
however, is extremely rare. Occasionally it is an arterio¬ 
sclerosis with multiple miliary softenings, and still more 
frequently examination of the brain shows vascular stasis, 
blocking of veins and capillaries, which may, in rare cases, 
proceed to thrombosis of the large veins opening into the 
longitudinal sinus, and cause red softening. The most 
frequent cause, however, is the characteristic chronic inflam¬ 
matory affection of the cerebral cortex of typical general 
paralysis, with marked irritative cell proliferation of the 
capillaries and within the perivascular lymphatics. Where 
the degeneration of the pyramidal tract is unilateral, or more 
marked on one side than the other, there is invariably a 
greater wasting of the corresponding hemisphere, which 
contains the cells from which these fibres take their origin. 
In no case does the examination of the cortex show that the 
changes are solely of vascular origin ; the atrophic process is 
partly due to chronic progressive atrophy, and partly due to 
acute degeneration. Thus we find the tangential fibres 
absent or greatly diminished in the prefrontal region of both 
hemispheres in cases where there is only unilateral pyramidal 
degeneration and unilateral fits. The cortical changes will 
be referred to in fuller detail later on. It may, however, be 
remarked that in all cases where there have been prolonged 
epileptiform seizures of recent, but not too recent, date, 
Wallerian degeneration in the pyramidal systems was found. 



Each seizure, whether maniacal or epileptiform, connotes 
cerebral irritation, vascular reaction, with cell proliferation 
and acute neuronic destruction, consequently a series of 
seizures will be followed by a series of degenerations. The 
appearance presented, however, by the degenerated fibres is 
not quite like that produced by experimental lesions. A 
section of the pyramidal tract stained by Marchi method 

Pig. 45. 

Photomicrograph of the right crossed pyramidal tract upper dorsal region 
of cord (Case 54). Marchi staining ; magnification, 750. The smaller inter¬ 
vening undegenerated fibres are partly commissural ground fibres. 

shows normal fibres, N ; fibres in which the sheath stains 
black, but still retaining an axis cylinder, E D ; others black 
throughout, indicating complete degeneration, D; lastly, 
empty spaces, indicating destruction of a fibre and absorption 
of the products. The smaller black degenerated fibres may 
be terminal branches of the pyramidal fibres. 

In those cases of tabo-paralysis in which the disease is 
characterised principally by a slow progressive dementia 



without epileptiform seizures, and in which microscopical 
examination shows a chronic atrophic degeneration of the 
neurons, affecting especially the molecular layer and the 
small and medium-sized pyramids with the corresponding 
atrophy of their association fibres, there is very seldom (and 
when present but very slight) Marchi reaction of degeneration; 
likewise there is no Marchi reaction of degeneration in the 
posterior columns in cases of chronic tabes dorsalis. Many 
of the spinal cords of these cases of tabo-paralysis were 
remarkably small, some not any larger than that of a child of 
two years (Cases 31, 52, 57), and this small size can only be 
explained by supposing that there is a general failure in the 
metabolic processes of nutrition of the nervous system. 
In tabes dorsalis the dwindling in size of the myelin sheath 
and its eventual disappearance, usually without any evidence 
of the Marchi reaction, makes one believe that there is a slow 
progressive process of failure in constructive metabolism of 
the neurons. The myelin sheath, together with the col¬ 
laterals, which are the latest development of the neurons 
embryologically, are the first to suffer; and why in one case 
the brain, in another the cord, or in some both fail, can only 
be explained by the intervention of some contributory factors 
which determine a locus minoris resistentice, such as vascular 
supply, stress, and heredity. 

Changes in the Anterior Horn Cells. 

In advanced cases of tabes, various deformities arise in 
consequence of amyotrophy; the small muscles of the hand 
and foot are specially affected, also the muscles of the leg, 
particularly the peronei and dorsal flexors, giving rise to 
various forms of club foot. Electrical examination of the 
muscles usually shows no reaction of degeneration, but in 
rare instances, e.g., Case 49, it does. Occasionally this may 
be due to chronic lead poisoning, as described in a case by 
Redlich, who claims that a typical posterior column degen¬ 
eration of tabes was produced by lead poisoning, independent 
of syphilis; associated with it, however, was a chronic 
anterior polio-myelitis. 

Some cases of progressive general paralysis apparently are 



due to chronic lead poisoning, and the fact that a tabic 1 lesion 
of the cord can be produced by this cause, tends to support 
the unity of the two diseases. 

It is only in advanced cases of tabes that one finds 
changes in anterior horn cells, and it is probable that these 
changes are due to total destruction of the sensory neurons 
which are in relationship with them. Warrington has shown 
that section of a large number of posterior roots produces 
chromolytic changes in these cells. I have been rather 
astonished at not finding more evidence of this in tabes and 
in the sections which I have prepared from cords of animals 
in which posterior roots have been cut. Possibly this was 
due to the fact that the animals were kept alive a much 
longer time than those of Warrington. Again, in cases of 
tabes, where there has been a very complete degeneration of 
the posterior roots, I have failed to find these chromolytic 
changes ; but when such have been seen (besides the 
destruction of the posterior roots), there was a very marked 
atrophy of the endogenous fibres of the posterior columns. 
This atrophy prevents stimuli entering from other regions in 
which the roots have not been completely destroyed, and 
marked changes, indicating progressive nutritional failure and 
even, rarely, atrophy of the anterior horn cells may occur. 
A similar condition of the cells was observed in a case of very 
chronic rheumatoid arthritis, with muscular atrophy. All 
the muscles responded to electrical stimuli, but owing to the 
joint affection, a progressive change, presumably, took place 
in the anterior horn cells ; their dendrons were broken off, the 
cytoplasm contained an excess of pigment and a diminu¬ 
tion of the Nissl bodies. 

In Case 49 of tabes, in which the change in the anterior 
horn cells was most pronounced, the cells exhibited the 
following characters. In the lumbo-sacral region, especially 
at the level of the first sacral, the anterior horns show the 
cells having their processes broken off; there is a perinuclear 
chromatolysis and marked excess of pigment. There is no 
marked proliferation of the intervening glia substance, as the 

“ Tabes Dorsalis und chronische Blei-vergiftung.” Wiener Medicinische 
Wochenschrift , 1897. 



accompanying photomicrograph shows. This case was one 
of arm tabes, and many years before he died the notes state 
that there was complete analgesia and anaesthesia of the 
arms, a very unusual condition in tabes, as the anaesthesia 
very rarely extends to the distribution of the upper cervical 
roots. Then it was noticed that there was a progressive 
wasting in the small muscles of the hand, more marked on 
one side than the other, with eventually reaction of degen¬ 
eration. Microscopic examination of the cord in the cervical 
regions showed an atrophic degeneration of the anterior horn 
cells in the upper two dorsal and last cervical segments, with 
a complete absence of fibres in the posterior roots and pos- 

Fig. 46. 

Case 49.—Amyotrophic tabes, anterior horn cells, first sacral segment 
showing chronic degenerative changes, breaking off of processes and excess 
of pigment. Magnification 300 diameters. 

terior columns of the segments of the spinal cord which 
correspond to the origin of the fibres which enter into the 
formation of the brachial plexus. There was a considerable 
atrophy of fibres also in the upper cervical segments; 
probably, therefore, owing to the accompanying destruction of 
the ascending and descending endogenous system of fibres in 
the posterior columns, all direct and indirect reflex spinal 
stimulus to the anterior horn cells had been abolished for 
many years. 

We can explain amyotrophic tabes in two ways: either 
the atrophy of the anterior horn cells has been brought about 
by a superadded chronic polio-myelitis, or the extreme tabic 



atrophy of the sensory neurons, which are in relation with 
those segments, has given rise to a secondary trophic change 
from the abolition of the stimuli incidental to their vital 
activities, similar to that which occurs in the sensory neurons 
after amputation of a limb. This latter hypothesis seems 
probable, even though we found in the small muscles of the 
hand the very unusual condition of electrical changes; but 
then the affection was essentially the same as in the 
small muscles of the foot, only of longer duration. The 
microscopic changes met with in the first sacral and ulnar 
segments of the cord were essentially the same, although the 
latter was more advanced. 

Why are the small muscles of the hand and foot so 
frequently affected by this amyotrophy, as compared with 
the large trunk and limb muscles'? The latter may derive 
some reflex tonus by impulses descending from the cere¬ 
bellum, partly incited by afferent impressions from the semi¬ 
circular canals (vide experiments of Bickel and Ewald) partly 
by peripheral afferent impressions transmitted by the 
posterior roots through Clarke’s column to the ventral and 
dorsal cerebellar tracts, which are cut off in tabes. 

Again, we have seen that an important association system 
of descending endogenous fibres of varying lengths exists in 
the posterior columns, that it is seldom entirely destroyed 
(only in the most advanced cases), and that these fibres in 
the dorsal and upper lumbar region are brought into rela¬ 
tion with the anterior horn-cells and the cells of Clarke’s 
column at different levels, consequently stimulus may enter 
the cord in regions where roots are, in the vast majority of 
cases, still partially preserved. By means of these associa¬ 
tion fibres of the posterior columns distant neurons in 
Clarke’s column and in the anterior horns may be affected, and 
thus preserve their nutritional and functional activity, and 
a certain amount of reflex spinal and reflex cerebellar tonus 
of the muscles. This is probable, seeing that the distri¬ 
bution of cutaneous anaesthesia and the microscopic exam¬ 
ination of the roots and spinal segments of a large number 
of the cases which I have recorded indicate that the roots 
which longest maintain function and structure are the cer- 



vical above the seventh, the lowest dorsal and upper lumbar; 
while the regions most likely to be affected are the lowest 
lumbar and upper sacral, the upper dorsal and the lowest 
cervical ( vide figs. 3 and 4). 

It was only in a case of arm tabes where there was 
during life evidence of affection of all the cervical roots by 
a complete anaesthesia of the arm that an amyotrophy in the 
upper limb was observed, although it was noticed several 
times in the foot. When it occurred in the foot there was 
always a very marked degree of analgesia and anaesthesia of 
the legs, indicating a very complete posterior root destruc¬ 
tion in these regions. These synergic association systems 
subserve spinal co-ordination, and their degeneration plays 
an important part in the later stages of tabes. 

Changes in the Optic Nerves. 

In eight out of twenty-eight fatal cases (nearly 30 per 
cent.) there was optic atrophy with blindness. Microscopical 
examination of the optic nerves was not made in a good 
number of the cases, therefore exact statistics cannot be 
quoted, but probably 60 per cent, of the cases would show 
some degree of optic atrophy. The clinical history of some 
of the cases would suggest that the optic atrophy is not 
always primary, but may in some instances be due to 
syphilitic basic meningitis. Microscopic examination, how¬ 
ever, does not help to decide. In several cases in which 
there was no definite naked-eye optic atrophy, one found a 
diffuse degeneration by Marchi method, also a large number 
of empty spaces as if fibres bad disappeared. Case 54 was 
remarkable in the fact that the optic nerves were smaller 
than natural, yet microscopically showed no overgrowth of 
glia tissue. The component fasciculi of the nerves were 
small, as if there was a general atrophy as inexplicable as 
the small spinal cord so frequently met with. In several 
advanced cases the retina was examined (vide Case 65). 

Developmental Defects. 

In three cases (41, 46 and 61) out of the twenty-eight 
examined there was a true heterotopia spinalis. As I have 



examined a very large number of spinal cords, normal and 
abnormal, but have never met with this condition except in 
these three cases of tabo-paralysis, it must be something 
more than coincidence that 10 per cent, of tabo-paralytics 
should have this defect; it supports the opinion of those 
who maintain that an hereditary deficiency may be an 
important causative factor in the production of the disease. 

Morbid Anatomy of the Brain. 

The changes in the brain in tabo-paralysis do not differ 
essentially from those of ordinary paralysis, except that, 
generally speaking, they are not so advanced, and are of a 
more chronic nature. 

Pachymeningitis was rarely met with in these cases ; the 
brain was seldom greatly wasted, and if it were so, it was 
generally one hemisphere which was markedly affected, due 
to acute vascular changes affecting extensively one hemi¬ 
sphere, associated during life with epileptiform seizures and 
hemiparesis, aphasia, and, occasionally, hemianaesthesia and 
hemianopsy. The pia-arachnoid membranes were thickened 
in proportion to the atrophy in the usual situation—the 
fronto-central regions, but the thickening was seldom very 
marked. In some cases the naked-eye signs were so slight 
as to require microscopical examination for confirmation, and 
in these the clinical symptoms were usually hallucinations 
and delusions with little dementia. The dementia, as pointed 
out by Dr. Bolton, was found usually proportional to the 
degree of wasting, but not always. The most marked 
changes in these early cases was found both macroscopically 
and microscopically in the orbital and pre-frontal regions, 
which occasionally exhibited a granular surface like a 
cirrhotic kidney. 

The lateral ventricles were dilated in proportion to the 
atrophy of the hemispheres. In several cases there was 
marked dilatation of the posterior part of the lateral ventricle, 
so that it extended within half an inch from the tip of the 
occipital lobe. This was found to be due to atrophy of the 
fronto-occipital and temporo-occipital fibres especially. The 
ependyma was usually granular, but not in the early cases; 



the fourth ventricle exhibited dilatation of the lateral sacs, 
and granulation of the surface in every case. This condition, 
however, is met with, and, indeed, all the other naked-eye 
signs to some degree, in all cases of chronic insanity with 
wasting, but it is seldom that one finds granulation of the 
floor of the fourth ventricle covering the calamus scriptorius 
in any other affection than progressive paralysis; it was 
present in even the earliest cases of tabo-paralysis; when 
there was no appearance of granulation in the lateral ventricles 
it was found in this situation. In other brain diseases, in 
which there may be just as much wasting of nervous tissue, 
there is nothing like the same amount of ependymal change, 
consequently in this disease, progressive paralysis, there must 
be some difference in the cerebro-spinal fluid or the capacity 
of formative reaction of the lining epithelium and glia tissue 
to account for this excessive granulation. I regard this, like 
the filling up of the central canal of the spinal cord, as an 
exaggerated formative proliferation of embryonic and glia 
tissues brought about by irritation, and this fact is of 
importance when placed by the side of other facts denoting 
bio-chemical toxic irritation. 

Vessels .—As I have shown elsewhere, if all the vessels 
of the brain, even in young people suffering with paralysis, 
be pulled out and washed with water, a few nodular patches 
of atheroma can be found in a considerable number of the 
cases, but this change may be regarded as merely a sign of 
previous syphilitic infection, and plays no part in the 
pathology of the morbid process. Only in cases of people 
who have passed 45 does one find any really marked change 
in the cerebral vessels, and then it is doubtful whether this 
change plays any important part in the production of the 
morbid process; it is merely a sign of pre-senile decay, and 
probably of the action of the syphilitic virus, especially 
when considered by the side of another fact, namely, the 
presence of atheroma of the aorta—a pathological condition 
found in the great majority of cases of progressive paralysis 
—more than 80 per cent. This condition is found even in 
young juvenile cases. 

In none of the twenty-eight cases referred to in the 



synopsis was there noted thrombosis of the veins opening 
into the longitudinal sinus, causing red softening ; this, 
however, I have seen in cases of progressive paralysis giving 
rise to epileptiform seizures, unilateral or bilateral, according 
as the process affected one or both hemispheres, and followed 
by hemiplegia, first of one side, then of the other, causing 
death, usually with hyperpyrexia. Syphilitic endarteritis 
was not met with in any of these cases, but I have seen it 
several times in cases of progressive paralysis. 

Microscopic characters of the disease may be considered 
under three headings :—(1) Changes in the nervous ele¬ 
ments, cells, and fibres ; (2) changes in the glia tissue ; 
(d) changes in the vessels. 

(1) I do not propose to give a long description of the 
changes met with in the nerve-cell, for they in no way 
differ from those met with in ordinary paralysis, and these 
changes are admirably described by Dr. Watson. 

Comparing, however, a large number of sections of 
experimental anaemia, tabo-paralysis, and general paralysis, 
I have formed the conclusion that the changes in the nerve- 
cells are of two kinds, acute and chronic; that the chronic 
process begins in the superficial layers of the cortex, small 
and medium-sized pyramids, and the molecular layer. The 
changes are slow and insidious; the cells and their fibres 
undergo an atrophic process without any marked inflamma¬ 
tory reaction. The acute process, on the other hand, occurs 
in paroxysms, and is associated with the formation of an 
acute irritant toxin having a local action, and causing, 
partly by its own chemical properties and partly by the 
inflammatory reaction of the vessels with capillary obstruc¬ 
tion, an acute coagulation necrosis of the cells very similar 
to that produced by ligature of the four arteries supplying 
the brain in cats and monkeys, which is invariably followed 
within twenty-four hours by a fatal result, preceded by 
epileptiform fits. (Dr. Leonard Hill’s experiments.) 

The cells stain diffusely, the Nissl granules are absent, 
and the chromophilous substance takes the form of a fine 
dust throughout the cytoplasm, the achromatic substance 
not being visible as the whole of the protoplasm is stained. 



If Unna’s polychrome or a mixture of methylene blue and 
saffranine be used, the cells are stained a pinkish purple, 
indicating an acidophil, instead of basophil reaction. 

The nucleus is often swollen up and clear, the nucleolus 
staining deeply by contrast. 

I have observed that the small and medium-sized pyra¬ 
mids, in cases with acute symptoms terminating fatally, 
show a very similar condition to that which I have observed 
in acute fatal experimental anaemia—namely, the nucleus 
swollen like a bladder to five or six times its size, clear, and 
surrounded by a thin film of cytoplasm ; the «ucleolus 
deeply stained, the intranuclear network faintly. In pro¬ 
portion to the destruction of the nerve-cells, there is, as a 
rule, but not necessarily, an overgrowth of glia-cells and 
vascular changes, which will be shortly considered. 

The neurons may be entirely destroyed, or only a small, 
irregular, triangular mass of protoplasm be left; or the 
larger processes may still persist, but present no Nissl 
granules, and exhibit no dendritic processes. Often the 
apical process is like a corkscrew; this condition I have 
found in imbecile brains, and I look upon it as evidence of a 
chronic process of atrophy. 

Such morbid conditions destroy the normal lamination 
of the cortex and the characteristic columns of Meynert. 

Occasionally I have observed cells with a nucleus under¬ 
going division ; this I have seen in absinthe poisoning, and 
I regard it as a sign of intense irritation. Salaman, in the 
first volume of the Archives, described a case of tabo- 
paralysis, in which he observed division of the nucleus in the 
cells of the posterior spinal ganglion. 

As Tuczek pointed out, atrophy of the tangential and 
supraradial fibres is the earliest and most constant microscopic 
change met with in general paralysis. None of the twenty 
cases which were examined failed to show this change to 
some degree ; but I do not remember one case in which the 
Marchi method showed recent degeneration of the tangential 
system. Possibly the method does not lend itself to show¬ 
ing destruction of these very fine fibres—more likely, however, 
it is that the process has taken place, and the products of 



destruction have been absorbed, or that as in tabes, the 
process is slow and progressive. When atrophic changes in 
these fibres could not be discovered in other regions of the 
brain, they were invariably found in the prefrontal, and 
usually in Broca’s convolution. Many of these cases showed 
a marked atrophy of the tangential system in the ascending 
parietal and the paracentral lobule, more marked than in the 
ascending frontal. I thought possibly this might be asso¬ 
ciated with the fact of the degeneration of the afferent 
system, but Campbell has shown that the ascending frontal 
normally possesses a greater wealth of tangential fibres than 
the ascending parietal; it is likely that this is associated with 
the presence of the Betz cells, the apical processes of which 
terminate in a panniculus, as shown by Cajal, in the molecular 
layer. It was frequently noticed that in one section there 
would be a considerable local disappearance of tangential 
and supraradial fibres, and we must account for this by the 
fact that there was a local atrophy of cells corresponding 
thereto. In fact, Nissl preparations clearly show this, and 
frequently there is not a uniform disappearance of cells in 
the superficial layers, but frequently little foci of atrophy. 

In Case 28, which we may consider as either one of tabes 
commencing with a mental crisis, or as tabo-paralysis with 
arrest of the cerebral disease and progress of the spinal, this 
unequal destruction of the tangential and supraradial fibres 
was especially observable. In that case, moreover, page 23, 
the atrophy and thickening of the membranes (see Plates I. 
and II.) were much more marked over tbe ascending parietal 
in its upper part than the corresponding portion of the 
ascending frontal. There were no acute changes in this 
case, and the superficial cells, beyond a certain amount of 
diminution in numbers and therefore thickness of lamination, 
presented no abnormal appearances. This was the only case 
observed which would at all correspond with cortical changes 
in tabes to which Jendrassik first called attention. Many 
people think that his cases were really tabo-paralytics, and I 
see no reason why they should not have been. For if Case 
28 had died in the attack of mania, I should certainly have 
described it as a case of tabo-paralysis; instead of this, he 
survived thirteen years. 



The atrophy of these superficial fibres is by no means 
limited to the fronto-central regions, although it is more 
marked there as a rule. Every part of the cerebral cortex 
may exhibit this change and sometimes it was found marked 
in the angular, temporal and occipital regions. In advanced 
cases, the interradial and, to a less degree, the radial fibres,- 
were found atrophied, but as a rule these were not affected, 
excepting in cases of marked wasting of the brain. In 
staining by the Weigert method it was often found that the 
myelin did not take the stain readily, behaving in this respect 
like foetal or infantile tissue and agreeing also with what was 
noted about the difficulty of staining the spinal cord in some 
of the cases. By the Marchi method the radial fibres were 
often found in a process of acute degeneration, especially 
where there was marked wasting of one or both hemispheres 
and signs of acute vascular changes. Such cases were found 
to show marked recent degeneration in the pyramidal systems 
in the cord, and indicated an acute death of the large Betz 
cells, from which these pyramidal fibres proceed. But we 
have seen that in twenty cases of the twenty-eight, there 
was degeneration and sclerosis of the crossed pyramidal 
tracts in the cord which could not be followed higher than 
the lower or mid-dorsal region. We can only account for 
this by a nutritive failure of the psycho-motor neurons, a 
chronic atrophic process affecting the most outlying portions 
of the neuron, most remote from the central seat of trophic 
influence, the nucleus of the cell. This presumably slow 
degenerative process of the crossed pyramidal tracts cannot 
be explained by any vascular or local condition of the spinal 
cord, or other long tracts in the lateral columns would be 
affected. The only explanation to my mind is the one I 
have given. 

(2) Glia ‘proliferation .—This is so very completely de¬ 
scribed by Dr. Watson that I need not do more than say 
my observations, made subsequent to bis investigations, 
confirm the results which he has described. I hope to 
publish shortly also observations showing that atrophy 
produced by experimental lesions can produce active glia 
proliferation. There is one point, however, in connection 



with glia formation which is not dealt with by Dr. Watson, 
and this relates to the evidence that the cerebro-spinal fluid 
in progresssive paralysis may contain some substances which, 
by irritation, produce formative proliferation. In three cases 
there was heterotopia spinalis; in one, Case 46, a careful 
Study was made of the changes in the epithelium lining the 
dilated canal. By the Marchi method the epithelium was 
seen to contain numbers of black particles, presumably 
products of fatty degeneration. By Mallory stain a formative 
proliferation was apparent in this epithelium, not limited to 
the posterior surface where the tabic process in the posterior 
columns was adjoining, but affecting the whole epithelium. 
I mention this latter fact because it supports the view that 
this active formative proliferation was not related to a 
substitution process, but rather to an irritant action of the 
fluid contained in the central canal. It will be remembered 
that this case died in epileptiform seizures, and, as I will 
shortly point out, an acute vascular irritant formative pro¬ 
cess is the most significant of all the signs of progressive 
paralysis. Examination of this epithelium (see photomicro¬ 
graph, Plate VIII., fig. 1) shows the nuclei of the cells 
undergoing an active proliferation; the nuclei, on account 
of the chromatin they contain, were deeply stained blue, 
and surrounded by a granulous pink-staining protoplasm, 
resembling the spongio-blasts of the embryonic tissue of 
the central nervous system. 

The nuclei of these spongio-blasts can be seen dividing to 
form two or even a column of cells. From the base of the 
epithelial cells long fibrous strands, passing deep into the 
substance of the cord, can be seen, and in the spaces inter¬ 
vening these embryonic glia cells are packed. I could then 
trace, proceeding outwards from the central canal, successive 
changes in the appearance of the glia cells very similar to 
those described by Dr. Watson. 

It is a well-known fact that in most chronic nervous 
diseases, and in old people, the central canal becomes filled 
up, but in quite young people suffering with general paralysis, 
or with Congo sickness, diseases in which there is other 
evidence of intense irritation, the central canal becomes 


filled up, and its place marked by a great number of 
embryonic glia cells, similar to those which I have described 
above. The epithelium lining the canal, from which pre¬ 
sumably these cells originated, has disappeared, owing to, 
probably, the pressure and consequent atrophy caused by 
proliferated glia cells. 

(3) Vessels .—The most constant and striking change 
which can be observed in progressive paralysis is afforded 
by the appearances presented by the vessels. Under a low 
power in an acute severe case of this disease there is such a 
proliferation of cells on the vessel walls and in their surround¬ 
ing lymphatics, which stain deeply with basophil dyes, that 
it almost appears as if the stained substance which was 
previously contained in the neurons had been transferred 
to these cells around the vessels. The more acute the symp¬ 
toms and the more rapid the progress of the case, the more 
obvious is this vascular change. What is it ? What does it 
signify ? 

Vogt has stated that plasma cells, which he regards as 
altered lymphocytes, are the cause of such an appearance of 
the vessels, and pathognomonic of the disease. 

Mahaim, on the other hand, considers lymphocytes patho¬ 
gnomonic of the disease; Havet, although he admits that 
plasma cells are found in general paralysis in nearly all 
cases, does not admit that they are pathognomonic. 

These plasma cells are not peculiar to the brain; they 
were first described by Unna, and he considered them 
as fixed tissue cells which have undergone proliferation. 
Marscholko has shown that they can be found in glanders, 
syphilitic granulomata, tubercle, lepra, carcinoma, and other 
diseases ; and he believes they are altered lymphocytes. 

The experiments of Cornil and Kanvier in the recently 
published edition of their “ Pathology,” show that irritation 
of the serous membranes by chemical substances can pro¬ 
duce a proliferation of the endothelial cells in all respects 
resembling these plasma cells. 

Pappenheim has recently introduced a differential stain 
whereby the nuclear chromatin substance is stained green 
and the surrounding granoplasm of the cell pink. 



The ordinary Nissl method for staining nervous tissues 
was used by Vogt, thionin by Havet. Unna’s polychrome 
is useful also, for it stains the granoplasm pink, the chromatin 
substance purple. 

The Unna-Pappenheim stain, when it succeeds, shows 
more clearly than any other the morphological characters of 
the plasma cells; also their close relation to lymphocytes. 

Lymphocytes .—The nuclear network of the lymphocyte 
is stained green ; from a central nucleolus, like the spokes of 
a wheel, fine strands of chromatin extend to the nuclear 
membrane, ending generally in little knots. The nucleus, 
as a rule, is surrounded by hardly any cell protoplasm. 
Lymphocytes are not often seen in the blood contained in 
the vessels, but single, in pairs, or groups, in the perineuronal 
and perivascular spaces, in the cerebro-spinal fluid and 
subarachnoid space. They occur in normal brain tissue. 
Occasionally lymphocytes may be seen with a certain 
amount of granoplasm stained pink, partially surrounding, 
like a half-moon, the nucleus. These may be transitional, 
and probably represent young forms of the plasma cells of 

Origin of the lymphocytes. — (a) The Blood. Dr. Pugh 
has found an increase of lymphocytes in the blood of 
epileptics during the fits. Dr. Boddington has kindly 
allowed me to refer to some unpublished observations which 
he has made, showing that during the second stage of 
general paralysis there is a considerable increase of the 
lymphocytes in the blood. 

Dr. Boddington’s Results. 

[It is not certain that the increase per cubic mm. is due to an arterial 
increase, as the total volume of blood nas not been measured ; but it is 
remarkable that in these conditibns it appears viscid, and flows with 
difficulty. ] 

This high percentage of polymorphonuclear cells during the seizures is a 
marked contrast to the condition found in cases of status epilepticus, in 
which, during the fits, there 'is an increase of mononuclear cells, chiefly 
lymphocytes, which latter may form 40 to 50 per cent, of the total. 

Immediately following the status there is an increase of polymorphonuclear 
cells, even up to 90 per cent. ; this, however, is quite transitory, lasting for 
twelve to twenty-four hours, whereas this high percentage in paralytic 
seizures continues for fourteen days, or more, and the return to the condition 
normal to the patient before his attack may take four or five weeks to 


accomplish. Myelocytes to the amount of 1 per cent, are seen in status 

In the second stage of general paralysis the blood differs from that of a 
healthy individual in that the percentage of mononuclear cells is increased so 
as to form 40 per cent, or more (in some few cases as much as 60 per cent.) 
of the total white cells, and of these considerably more than half are lympho¬ 

In the third stage there is an increase of polymorphonuclear cells,* which 
amount to 80 or 85 per cent, of the total white cells. 

In the convulsive seizures of the second stage there is a very marked and 
sudden increase in the total number of cells per cubic mm., so as to form in 
the course of a few hours six or seven times the normal number; and this 
increase consists almost wholly of polymorphonuclear cells, which form 90 to 
95 per cent, of the total. At the same time there is a total disappearance of 
eosinophils, and myelocytes appear in the blood. 

Examination of sections of the brain from a large number 
of cases of various diseases in which there have been fits 
prior to death, including five cases of status epilepticus, has 
shown the existence of excess of lymphocytes in the peri- 
neuronal spaces. These may come from the blood, but 
lymphocytes are not usually regarded as capable of active 
migration through the vessel wall. They may, however, be 
derived from lymphocytes normally existing in the lymph 
spaces of the tissues. Pappenheim regards this as probable. 
We may therefore conclude that the altered condition of 
the blood which is Associated with the fits may cause a 
stimulant and proliferative action on the lymphocytes of 
the blood, and especially at the primary seat of the morbid 
process—the brain. 

After examination (by one of the methods related) of an 
immense number of sections of the brain and spinal cord 
of the various forms of nervous disease and experimental 
lesions enumerated below :— 

Twenty cases of experimental anaemia (dogs, cats and 
monkeys), by Dr. Leonard Hill. 

Cases of abrin, ricin and botulin poisoning, by Dr. Durham. 

One case of sunstroke. 

Two of pernicious anaemia. 

One stab in the heart (probably man suffering with acute 

One leukaemia. 

One exophthalmic goitre. 

* The polymorphonuclear cells may, however, be due to terminal infection. 
(F. W. M.) 



Two beri-beri. 

Five status epilepticus. 

Two acute alcoholism. 

Five alcoholic dementia and polyneuritis. 

Two amyotrophic lateral sclerosis. 

Five cases of juvenile paralysis. 

Twenty cases of tabo-paralysis. 

Ten cases of general paralysis. 

Two cases of Congo sickness. 

Two cases of multiple syphilitic gummata. 

I came to the conclusion that the plasma cells of Marscholko 
described by Vogt as pathognomonic of general paralysis, 
and which will now be described, are almost pathognomonic 
of this disease. I say almost, because I found them in a case 
of Congo sicknesss with fits (vide fig. 7, Plate XI.), and I 
failed to find them in one case of juvenile general paralysis. 
These cells contain a nucleus very like the nucleus of a 
fully-developed lymphocyte, viz., a central nucleolus with 
wheel-like strands of chromatin ending in four to seven 
knobs beneath the nuclear membrane. Like the nucleus of 
the lymphocyte, the chromatin stains deeply green, whereas 
the granoplasm around the nucleus is stained pink by 
Pappenheim’s method : very frequently there is a clear halo 
between the nucleus and the granoplasm. The plasma cells 
are of varying size, from 7 to 14 ft, they are polygonal, oblong, 
oval or triangular in shape; the green-stained nucleus is 
usually at one end of the cell; frequently two cells having 
their nuclei in opposition indicate cleavage. Many of the 
cells show an endogenous nuclear proliferation. The grano¬ 
plasm contains a fine dust of particles stained pink and no 
coarse granules, so that it has a grumulous appearance. 
These cells lie like a plaster on the vessel wall (vide figs. 3, 
5, 6, 7, Plate VIII.). 

In the neighbourhood of vessels so affected one always 
find a proportionally marked acute destruction change in the 

In some cases of tabo-paralysis in which there had been no 
fits, and death had occurred within a short time of the onset 
of mental symptoms, the prefrontal and orbital regions of 



the cortex alone may show naked-eye changes of the lesions 
characteristic of general paralysis, and it may be only in such 
regions that the plasma cells will be found. (Case 39, p. 156.) 

In cases where there has been marked spinal affection 
these cells have been found in great abundance around the 
vessels in Broca’s convolution, the island of Reil and the 
posterior third of the first temporal. (Cases 46 and 54.) 

We may associate their existence in abundance with 
intense irritation, increased neuronic irritability followed by 
degenerative destruction. The former case was not paretic 
in the limbs; his speech, however, was markedly affected, 
and facial paresis existed. Accordingly, marked plasma cell 
proliferation and acute neuronic destruction was found in 
Broca’s convolution and the lower part of the frontal and 
parietal convolutions, and but little in the second frontal and 
adjacent motor area. In Case 54, on the other hand, there 
was marked sensory aphasia, hemiparesis, and transitory 
hemianaesthesia ; plasma cells in abundance and acute cell 
destruction were found in the angular, supramarginal and 
first temporal of the left hemisphere. 

Plasma Cells proportional to Acute Neuron Irritation 
and Destruction. 

The plasma cells of Marscholko were found in all cases of 
general paralysis and tabo-paralysis examined; they were 
not found in the brain of any other of the conditions 
enumerated, with the exception of one case of Congo sickness, 
and one of multiple syphilitic gummata. They were not 
numerous in the Congo sickness, and required much search 
{vide fig. 7, Plate VIII.), although the perivascular lym¬ 
phatics throughout the whole central nervous system were 
crowded with lymphocytes in a way that I have never seen 
in any other disease. Sections of the spinal cord, medulla, 
and pons in tabo-paralysis and general paralysis did not 
shlbw these plasma cells around the vessels. 

They exist especially in those regions (fronto-central) of 
the brain which generally show wasting in general paralysis, 
and their abundance is clearly associated with the amount 



and the intensity of the acute neuronic irritation and 

Endothelial Cells as the Origin of the Plasma Cells. 

The endothelial cell proliferation is marked in all cases 
where there is active destruction going on. The nuclei of 
the capillaries increase in numbers and can be seen under¬ 
going mitosis. This proliferation of the endothelial cells 
W'ould tend to obliterate the lumen of these delicate tubules 
and obstruct the passage of red corpuscles, thus interfering 
with tissue respiration and the removal of the waste products 
of neuronic activity. Endothelial cells proliferate in the 
vessels of the spinal cord, or at any rate, there is an increase 
of the nuclei; but I have never observed plasma cells in the 
gray matter of the spinal cords of paralysis cases. A good 
way to study the endothelial proliferation of the capillaries is 
to make film preparations of fresh cortex squeezed between 
two cover-glasses (vide fig. 4, Plate VIII.). The capillaries 
can be traced into the venules; the proliferated endothelial 
cells can thus be determined. The walls are no longer clear 
with a delicate outline, but consist of a granoplasm with 
increased numbers of long nuclei. As you pass from the 
capillary to the venule the nuclei become more oval, and the 
proliferated cells take on the form of plasma cells: but it 
may be argued that these cells may arise from the endo¬ 
thelial cells of the lymphatics surrounding the small venules, 
or lymphooytes contained in the sheath. 

I have observed plasma cells in the perineuronic spaces 
and in the tissue away from vessels; moreover, the much 
closer resemblance of the nucleus of the lymphocyte in shape 
and arrangement of the chromatin, together with the oc¬ 
currence of transitional forms between lymphocytes and 
plasma cells, inclines me to alter my original opinion and 
conclude that the balance of evidence is in favour of the 
plasma cells being derived from lymphocytes and not from 
endothelial cells, although the latter undoubtedly undergo 
active proliferation. 

The proliferated endothelial and plasma cells seem to 



have a phagocytic function, for we can find blood pigment in 
various stages of disintegration and chemical change within 

What is the pathological significance of these plasma cells 
in the brain in general paralysis ? 

The clinical symptoms associated with the anatomical 
findings undoubtedly show an intense irritant morbid process, 
followed by acute neuronic destruction. But, as already 
remarked, plasma cells are found in many other morbid 
processes where acute irritation and destruction is occurring ; 
therefore in general paralysis they are only indicative of an 
acute irritative process in the brain. 

We have next to consider the source of the irritant, 
which, presumably, is of a bio-chemical nature, and produced 
paroxysmally by a localised conspiracy of factors', for if some 
toxin or autotoxin generalised in the blood were the sole 
factor, then we ought to find its effects manifested equally 
throughout the nervous system, but it is not. 

Those portions of the hemispheres, the veins of which 
drain into the longitudinal sinus, are the regions in which 
venous stasis is most apt to occur, for the following reasons: 
The blood flows against gravity; the veins embouch into 
the longitudinal sinus in a contrary direction to the current; 
the suction action of the thorax influences the flow from 
the lateral sinuses first; consequently violent expiratory 
efforts and suspension of respiration leading to cerebral 
congestion, or any general condition of venous plethora from 
portal congestion, would, owing to these mechanical dis¬ 
advantages, tend to stasis in the fronto-central regions. 
Again, the brain, being contained in a closed cavity, the 
quantity of blood in the organ is always the same, therefore 
if vaso-motor irritation causes sudden anaemia from diminu¬ 
tion of arterial supply, a proportional reflux of venous blood 
would take place and tend to flow into these regions. Now 
the portion of the brain most likely to suffer from sudden 
anaemia is the portion supplied by the internal carotid (viz., 
fronto-central), because the force of gravity would operate 
most on the blood contained in the distribution of this vessel. 
Therefore the morphological conditions of the arterial and 



venous circulation in the fronto-central regions favour 
anaemia and venous congestion. 

Slight faints and lapses of consciousness are among the 
earliest prodromal signs of general paralysis, and are indica¬ 
tive of these vascular disturbances. These, however, are 
subsidiary, but important exciting and determining factors 
in the disease. 

The paroxysmal character of seizures, followed by 
apparent betterment, the microscopical evidence of an in¬ 
tense irritative and destructive process more obvious than 
in almost any other brain disease, point to the formation in 
the blood of a toxin which fixes on to certain portions of 
the central nervous system, which either stress, heredity, or 
anatomical conditions place in a lowered state of resistance. 
If the vascular factor alone were a cause, heart disease 
should be a cause of general paralysis. The paroxysmal 
attacks in tabes, of lightning pains, of visceral crises, of 
mental crises, followed by intervals of relief, all point to 
some coming and going of an irritant which acts upon 
decaying structures. 

The mania and grandiose delusions which frequently sub¬ 
side, and the paroxysmal character of the epileptiform seizures, 
point to the formation of a toxin or accumulation of a toxin 
in the blood, which produces an effect, but is destroyed to 
accumulate again. The observations of Krafft-Ebing strongly 
support the view that general paralytics possess an immunity 
to syphilis; it may be presumed that the effects of the toxin 
are still in operation. He inoculated eight general paralytics, 
who exhibited no signs of syphilis, with the virus of a hard 
chancre, and they showed no signs of infection subsequently 
when watched for 180 days. 

As in diphtheria, the general toxic action of syphilis 
altogether overshadows, and, indeed, often bears no propor¬ 
tional relationship to the local effect of the contagium, 
especially in the late after-effects. Experiments of Ehrlich, 
confirmed by Bulloch, seem to show that there are a mixture 
of bodies in the crude toxins of diphtheria. Likewise 
Ehrlich and Madsen have shown that certain bouillon 
cultures of the tetanus bacillus may contain two toxins, a 



tetano-lysin, and the ordinary spasm producing body tetano- 
spasmin. Unfortunately, owing to the absence of our know¬ 
ledge of the specific germ of syphilis and the immunity of all 
animals to infection, it can only be deduced by analogy that 
Hitzig is probably right in supposing that the syphilitic virus 
may convey several poisons, one of which may be latent, and 
produce these late manifestations, tabes and general paralysis. 
Like diphtheritic paralysis, these late nervous manifestations 
bear no necessary relation to the primary local and general 
constitutional manifestations accompanying the disease. The 
only difference in the analogy between syphilis and diph¬ 
theria is the much slower evolution of the symptoms of 
the former, and it may be added, as a result, the life-long 
immunity conferred thereby. 

Is it therefore warrantable upon the facts to hypothe¬ 
cate a latent toxin of syphilis which has a special affinity 
for nervous structures—a toxin which can only operate 
under certain abnormal metabolic conditions of the neurons. 
In Professor Welch’s most illuminating Huxley lecture he 
thus referred to the work of Ehrlich and Preston Kyes :— 

“ Preston Kyes, working in Professor Ehrlich’s laboratory, in 
an investigation just published on the mode of action of cobra 
venom, confirms the conclusion of Flexner and Noguchi concern¬ 
ing the amboceptor nature of cobra venom. ... Of great 
significance is the demonstration by Kyes of still a third 
substance, namely, lecithin, which is capable, through combina¬ 
tion with the venom intermediary body, of completing the 
haemolytic potency of venom. . . . The suggestion by Ehrlich 
and Kyes that possibly the cholin group is the toxophore group 
of lecithin is interesting. . . . 

“ Flexner and Noguchi have demonstrated experimentally 
that, like the haemolytic, so also the leuco-toxic, neuro-toxic and 
other cyto-toxic properties depend upon combinations of venom 
intermediary bodies, with complements contained in the cells 
poisoned by venom, or in the fluids bathing these cells. The 
positive demonstration by Preston Kyes of a special class of 
intracellular complements or endo-complements is unquestionably 
of great pathological interest, and seems destined to play an 
important part in many morbid conditions, both with endogenic 
and exogenic intoxication.” 



The products of degeneration of nervous tissues are 
numerous, and consist not only of cholin, but a number of 
bodies of the lecithin group, being various derivations of 
protagon. Cholin is the most easily separated and recog¬ 
nised physiologically and chemically, and it is possible that 
the products of degeneration vary according to the cause 
and nature of the destructive process. Still there is no 
evidence to show that these products of degeneration can 
per se produce the clinical manifestations and morphological 
changes indicating neuronic irritation and destruction of 
general paralysis, otherwise we ought to get these changes 
in other diseases, also desttuctive lesions of the nervous 
system. Therefore I think it may be conceived as possible 
that there is a latent toxin in the blood which combines with 
endo-complements the products of deranged neuron activity, 
producing locally (that is, where the neuron metabolism is 
deranged either by stress, circulatory deficiencies, or heredi¬ 
tary physiological or anatomical defects) an active neuro- 
lysin proportional to (a) the amount of latent toxin in the 
blood, and ( b ) tbe amount of endo-complement produced by 
deranged neuron metabolism. The glia-cell, lymphocyte and 
endothelial cell proliferation and the presence of abundance 
of plasma cells are tbe signs of the local vital reactions of 
the tissues to this poison and proportional to its amount and 
intensity. Where nervous tissues are latest developed and 
most unstable, where venous stasis and anaemia are most 
likely to occur, and in those structures which are subjected 
to the greatest physiological activity, there is defective meta¬ 
bolism to be found, and there, on this hypothesis, is formed an 
active toxin-producing irritation and destructive local effects. 
Tbe nature of the conspiracy of factors and the vital reaction 
of the tissues will determine the seat and extent of the acute 
neuronic irritation and destruction. 

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Plate VIII 

Fig. 1 . — Photomicrograph of a section of the central canal of the spinal 
cord with heterotopia, Case 46. The nuclei of the epithelial cells, with their 
chromatin network, can be seen proliferating; lower down they can be seen 
surrounded by protoplasm, and undergoing active division. A column of four 
nuclei surrounded by protoplasm is seen; the upper two nuclei show very 
clearly two asters, indicating the nuclear division which has occurred. 
Mallory stain. Magnification, 760 diameters. 

Fig. 2.— Photomicrograph of a section of the ascending parietal con¬ 
volution from Case 45, showing a small vein surrounded by plasma cells, 
which are lying in a dilated lymphatic. The vessel at another part had 
ruptured and filled the lymphatic sheath with blood corpuscles. Some of 
the large, swollen-up cells showed in their interior the blood pigment in 
various stages of destructive disintegration ; they appear to have, therefore, a 
phagocytic function. Nissl stain. Magnification, 500 diameters. 

Fig. 3.—Photomicrograph of a section of Broca’s convolution, Case 46, 
showing abundance of typical plasma cells of Marschalko. The cells are 
oblong, oval, polygonal, and triangular. The granoplasm is dark on account 
of its taking the pink dye. The nucleus is distinct, with its nucleolus and 
chromatin strands terminating in chromatin knobs. The nucleus is generally 
at one end of the cell, indicating active division. In some there is a clear 
halo around the nucleus. Many of the cells show endogenous nuclear pro¬ 
liferation. The cells are seen stuck on the vessel wall like the corrugated 
bark of a tree. At the lower end of the section the indistinct forms of the 
unstained red corpuscles are seen within the lumen of the cut vessel. Poly¬ 
chrome Nissl stain. Magnification, 750 diameters. 

Fig. 4. — Photomicrograph of a film preparation of the vessels stained by 
Nissl method from a case of general paralysis. It shows the proliferation of 
the nuclei of the capillaries, the absence of red corpuscles, and the obliteration 
of the lumen by the endothelial cell proliferation. Magnification, 500 

Figs. 5 and 6.—Drawings to show different types of cells around vessels in 
general paralysis; p = plasma cell, m = mastzell, 1 = lymphocyte. Magni¬ 
fication, 600 diameters. 

Fig. 7. —Photomicrograph of small vein, case of Congo sickness, stained by 
Nissl method, showing plasma cells. On account of the specimen being some¬ 
what faded, the negative was not strong; the ceils have been retouched, 
but it represents fairly accurately what could be seen. Magnification, 750 

Fig. 6. 

Tabes in Asylum and Hospital Practice, 

Fig. 5. 

To faoe p. S06. 

Fig. 2. 

Fig. 3. 



Fig. 4 



Notes upon the Pathology of Tabes and 

Leyden was the first to point out that the pathology of 
tabes depended upon the degeneration of the posterior roots 
and their intraspinal connections. Westphal, Dejerine and 
Oppenheim, among others, showed that the peripheral nerves 
were also affected; but most observers now agree with Leyden 
that the symptoms of tabes are especially due to the degen¬ 
eration of the central projections of the posterior spinal 

Every posterior root furnishes fibres to different sensory 
nerves of the periphery. The cutaneous surface is subdivided 
into zones or segments, of which each receives its sensory 
innervation from certain definite posterior roots. These seg¬ 
mental posterior root areas overlap one another, and each 
receives fibres from two or three contiguous roots. It will 
thus be manifest that the area of distribution of cutaneous 
anaesthesia will be quite different, when it depends upon 
alteration of the posterior roots and their intramedullary 
prolongations, to when it depends upon alteration of the peri¬ 
pheral nerves. In tabes, cutaneous sensory dissociation, 
especially in not very advanced cases, is the rule; whereas it 
is the exception for an anaesthesia of peripheral origin to 
exhibit the characters of dissociation. There is, however, 
not only dissociation of cutaneous sensibility, but also marked 
subjective and objective sensory disturbances of the deep 
structures, which may exist independently of cutaneous 
disturbances. We have already referred to the fact that 
probably the fine fibres of the posterior roots convey cuta¬ 
neous sensations, and the coarse fibres sensations from the 
deep structures; and we have seen, moreover, that clinical 
observations and morbid anatomy have demonstrated that 
these two systems may be affected independently. 

The interesting observations of Dr. Anderson upon the 
myelination of the different systems of somatic and 
splanchnic fibres are of great interest, and should help to 
throw light on some of the phenomena of this disease. He 
has shown that both somatic and splanchnic myelinated 
afferent fibres consist of two distinct sets, which develop 



their myelin sheath simultaneously in both splanchnic and 
somatic posterior roots and peripheral nerves; the two sets 
of fibres convey impulses respectively from deep structures 
and cutaneous or epithelial structures. 

Taking the myelinated splanchnic fibres, he finds that 
there is one set which has as its peripheral termination 
Pacinian corpuscles, contained in the structures of the 
abdominal viscera and larynx. These large fibres acquire 
their medullary sheath contemporaneously with the large 
myelinated fibres, terminating in the Pacinian corpuscles, 
muscle spindles and end-organs, which are contained in the 
deep somatic structures. The finer medullated fibres which 
terminate in the skin, and which are connected with pressure 
and painful sensations especially, are myelinated contem¬ 
poraneously with the fine set of medullated splanchnic 
afferent fibres, which, he argues, supply the epithelial 
structures of the viscera, and which would endow them with 
common sensibility. Anderson considers that there is a 
correlation between the function of the afferent splanchnic 
and somatic fibres, which have Pacinian corpuscles as end- 
organs. The irritation of these neurons, he considers, gives 
rise to the deep pains in the limbs and the pains of the 
visceral crises. 

Microscopic examination of the white rami shows that 
there are both large and small white medullated fibres 
contained in them; the large fibres correspond to these 
large splanchnic afferent fibres from the Pacinian corpuscles. 
The small fibres are partly efferent, arising from cells of the 
lateral horn of the intermedio lateral tract, which cells have 
their long axis directed horizontally, and are found in the 
thoracic region only, where this outflow of fine efferent 
medullated fibres takes place. Some of the fine fibres, 
however, are sensory fibres of the viscera, and subserve a 
protective function by virtue of the pain which intense 
stimulation, mechanical or chemical, might cause. 

Normally we feel no sensation from our internal organs; 
when painful stimuli are conveyed by the white rami to the 
posterior spinal ganglia, thence to the spinal cord, where 
these flow over into the terminals of the somatic skin 



neurons, they give rise to characteristic pains referred to 
morphologically correlated skin areas (Mackenzie, Head). 
Thus we may really have an illusion as to the true seat 
of the pain and the nature of the process occasioning it; 
our experience, however, will lead to its correction. 

Besides pain, there is rigidity of correlated muscles due 
to a protective reflex, by which the parts are kept as much 
at rest as possible. The severe pain accompanying it may, 
as Prof. Sherrington aptly says, be looked upon "as a 
psychical adjunct of this protective reflex.” The pain is, 
however, much greater in some individuals than others; 
not because the stimulus is greater, but because the sub¬ 
jective mental attitude of the individual, by a concentration 
of consciousness to the painful spot, is greater. But it 
might logically be asked, would it be possible to concentrate 
the attention on a viscus of which one has no knowledge by 
touch or sight, if it were not for the pain referred to the 
correlated skin area ? By no effort of the attention can we 
imagine the rythmical contractions which are taking place 
with phasic or periodic regularity in our ureters, bile ducts 
and gall bladders. It is only when they contract violently 
in response to intense irritation, that we are painfully 
instructed by experience and the referred pain, as to the 

A great deal of discussion has arisen as to whether the 
viscera are really painful. I think there can be no doubt 
that a peculiar dragging and sinking sensation is associated 
with irritation of the viscera, probably due to stimulation of 
coarse afferent fibres with Pacinian corpuscles, independent 
of the sensation in the skin areas. Many of the patients who 
suffered with gastric crises complained of a deep-seated pain 
within the abdomen, and no doubt this was due to irritation 
of the splanchnic afferent neurons which were undergoing 
destruction in the posterior roots of the mid-thoracic 

The accompanying figure (47) illustrates this point. 

Cases often attend hospitals for gastric troubles which 
are thought to be dyspepsia, whereas really they are very 
mild gastric crises. In severe cases there is no doubt intense 



irritation, generally with destruction of the sixth, seventh, 
and eighth posterior roots, conveying afferent splanchnic 

Fig. 47. 

Diagram to show somatic and splanchnic nervous structures in the 
seventh thoracic metamere. The correlation of the skin and muscle in the 
protective reflex is indicated. 

E.V.V. = Efferent splanchnic ; E.S. = Efferent somatic; A.V.V. = 
Afferent splanchnic ; A.S. = Afferent somatic ; S.P. = Plexus of Auerbach 
and Meissner ; E.V. = Efferent visceral from sympathetic ganglion; A.V. = 
Afferent visceral to sympathetic ganglion. 

The coarse and fine fibres which exist in both somatic and splanchnic 
nerves are not differentiated. 



impressions from the stomach (Case 31). The quality of a 
sensation depends on multiple circumstances—the nature 
intensity of the peripheral excitation, the state of the con¬ 
ducting neurons and of the cortical perceptive centres; but 
whatever be the cause of the objective sensation coming 
from the periphery, it is in the cortical terminus of the 
afferent system that the stimulus is perceived as a state of 
sensation of heat, cold, pain, contact or movement, and 
localised to a particular part of the body. The localisation 
is very often imperfect; this is explicable by the fact that 
each spinal segment of the grey matter of the posterior horns 
is correlated with a definite skin area. When all the sensory 
cutaneous neurons proceeding directly to that area have 
been destroyed, sensory impulses may still enter the cord, 
owing to the overlapping of adjacent roots in the nervous 
supply of that skin area, and the stimulus be referred to an 
area above or below. In the limbs, where the segmental 
character is obscured, the cause of this imperfect localisation 
is not so obvious. The wrong localisation is, however, 
due to a state of consciousness brought about by excitation 
of neurons in the wrong segment, and consequently is 
outwardly projected in the mind to that area of skin which 
is morphologically correlated with the segment excited. 

The subjective attitude of the individual (borrowing an 
expression of Mr. Shand) plays a very important role , not 
only in the subjective disturbances of tabes and tabo- 
paralysis, but also in the objective; for often the objective 
sensory disturbances are erratic and changeable. Thus, 
where at one moment a patch of anaesthesia or analgesia 
is found, a little later the same patch may be sensifacient, 
or even hyperaesthetic or hyperalgesic. This may partly be 
accounted for by summation of stimulus, or by the variability 
in the irritability and conductibility of the systems of spinal 
sensory neurons, but still more often to the subjective atti¬ 
tude of the individual—the state of consciousness which is 
especially related to the physiological activity of the cortex 

In tabes with insanity, we can therefore understand how 
’ acute the suffering of a patient is, when he concentrates the 



consciousness of an unsound, but still active, mind upon the 
pains and tortures, which he believes enemies and unseen 
agencies are working upon him. The effect on the mind 
is reflected in the physiognomy, which portrays misery and 

In tabo-paralysis, in the early stages, there may be an 
intensification of the pains and sufferings by the subjective 
attitude of the individual towards the effects produced by 
the irritation and degeneration of the sensory, somatic, and 
visceral neurons; and as we have said before, and given 
numerous illustrations thereof, such may cause pseudo¬ 
hallucinations, illusions and delusions. 

In the later stages of tabo-paralysis, as, indeed, in general 
paralysis, when the dementia becomes pronounced, the patient 
suffers very little or no pains, nor does he feel pain when 
pricked with a needle. The stimulus may be the same, but 
the effect on consciousness is diminished or lost by the 
partial destruction of the cerebral cortex. This probably 
explains the fact that such patients may often suffer with 
very painful diseases without any complaint. The absence 
of pain associated with physical signs of tabes suggests, 
therefore, cortical degeneration. 


Definition .—Coordination is the regulation and adjust¬ 
ment of the innervation currents flowing to correlated groups 
of muscles in such a way that the movement may be executed 
with precision in rate, force and direction, with the least 
expenditure of nervous and muscular energy. To attain per¬ 
fect coordination even in the simplest movement entails 
a vast complexus of functionally correlated neurons in the 
cortex, mesencephalon, cerebellum and spinal cord. 

The current of reciprocal innervation of correlated groups 
of muscles is dependent directly upon the outflow from cor¬ 
related groups of spinal-motor neurons, with which the 
muscles are in direct anatomical connection. 

The complexus of neurons which determines, controls, 
adjusts and regulates this mechanism of innervation is much 
more complicated than is generally supposed and taught. 



Every day new experiments and observations show fresh 
paths indicating groups of neurons with special functions. 
We may consider these groups, however, under three head¬ 
ings : 

(1) Spinal, afferent and efferent. 

(2) Cerebellar and mesencephalic, afferent and efferent. 

(3) Cerebral, afferent and efferent. 

These are represented as the nervous circles in the 
accompanying diagram, which, however, is considerably 
simplified. In each of these nervous circles there are 
complex association systems, especially in the cerebral. The 
spinal intercalary are not represented, nor are the neurons 
which convey impulses by the optic nerves to the mesen¬ 
cephalon and cortex, nor those coming from the semi¬ 
circular canals to Deiter’s nucleus. 

In tabes no two cases are exactly alike as regards the 
clinical phenomena and morbid anatomy, but there is a 



general resemblance in all, for of the 28 cases I have 
examined, the three sets of coarse fibres entering the 
posterior columns invariably showed simultaneous degenera¬ 

Reasons have already been advanced to show that these 
three sets of fibres, proceeding respectively to the spinal 
motor cells, to the cells of Clarke’s column, and to the 
posterior column nuclei, represent sensory channels in the 
spinal, cerebellar, and cerebral nervous circles. There is 
good reason to believe that the bulk of the fibres forming 
the columns of Goll and Burdach come from the small 
muscles of the hands and feet, and this is supported by the 
fact, which Sherrington has shown, that one-third to one- 
half the fibres entering muscle are sensory, and terminate 
in muscle spindles. The proportional degeneration of fibres 
in the spinal, cerebellar, and cerebral afferent systems varies 
according to tbe roots affected ; and the symptoms vary too. 

It has been shown (1) that in every case in which there 
was marked ataxy there was degeneration of the plexus of 
fibres around the cells of Clarke’s column. (2) That in 
Friedreich’s disease there is marked ataxy, no loss of 
cutaneous sensibility, not very much hypotonus, but a 
marked degeneration of the fine plexus around the cells of 
Clarke’s column, atrophy of the cells and of the ventral and 
dorsal cerebellar tracts. (3) Many cases of ataxy were met 
with in which there was little or no loss of cutaneous 
sensibility, but marked ataxy of the limbs. Again, the 
destruction of the coarse fibres in the lumbo-sacral region 
was usually much in excess of that of the fine fibre system 
of Lissauer’s tract. We therefore conclude that the cere¬ 
bellar afferent impulses play a most important part in co¬ 
ordination, and that the impressions coming from the 
deep structures are of more importance in coordination 
than those from the superficial structures. 

We can now consider the mechanism by which the 
neuron complex represented in the diagram consciously and 
semi-automatically regulates and adjusts the innervation of 
muscles. We are conscious of the position of our limbs by 
the sensory impulses arriving at the seat of consciousness, 



the cerebral cortex; and before a movement can be initiated 
ideation of the present position, followed by revival in con¬ 
sciousness of the position willed, precedes the outflow of 
impulses through the psycho-motor neurons. The accuracy 
of the kinsesthetic memory picture therefore determines the 
perfection of the adjustment and regulation of the efferent 
impulses concerned in the coordinate movement. The 
anatomical substratum of cerebral coordination is there¬ 
fore formed of all those neurons which convey sensory 
impulses from the periphery to the cortex, of the cortical per¬ 
ceptive neurons, and of the infinite combinations of associa¬ 
tion neurons lying between them and the psychomotor 
neurons, all of which give rise to the memory pattern which 
plays upon the terminals of the dendrons of appropriate 
groups of psycho-motor neurons, the efferent stimuli from 
which cause reciprocal innervation of correlated groups of 
spinal motor neurons, which in their turn preside over groups 
of synergic muscles. 

With the progressive evolution of the brain in the zoo¬ 
logical scale, coordination in successive movements depends 
primarily more upon cortical and less upon spinal action. 
In man, coordination is primarily cerebral, even in semi¬ 
automatic processes such as walking; all spinal coordination 
has not, however, disappeared, for the most perfect example 
of subcortical coordinate reflex is still left to man in the 
prehension of a new-born infant, as shown by the fact that 
it can support the weight of its body when grasping a bar. 

When the crura cerebri are divided in animals, viz., 
apes, decerebrate rigidity is produced ; the cerebral nervous 
circle is no longer in operation, only the subcortical circles; 
and certain phenomena of great interest can be demonstrated. 
If the skin of the palm of the hand be stimulated by dipping 
in hot water, a reflex coordinate movement of flexion on 
the side stimulated, and extension on the opposite side takes 
place. The movement so initiated persists —cataleptoid state, 
due to persistence of reflex spinal and cerebellar impulses. 
When the posterior roots are cut, this cataleptoid condition 
immediately disappears; consequently the continuance of 
nnervation which led to the cataleptoid condition, whether 



spinal or cerebellar, or both, depended upon incoming stimuli 
by the posterior roots (Sherrington). 

As the stimulus employed in this experiment was only 
temporary it is more reasonable to suppose that the persist- 
ance of the stimulus, which produced the continuance of the 
movement initiated by the cutaneous excitation, was due to 
incoming stimulus from the deep structures being put in a 
state of increased tension in the new position which the 
limb assumed. There is every reason why it should thus 
persist. The neurons transmitting the incoming currents 
from the contracted muscles are anatomically and function¬ 
ally correlated with the neurons which transmit the outgoing 
currents ; and the subcortical, spinal, and cerebellar nervous 
circles which are transmitting the most innervation currents 
will prevail. Probably this effect is mainly of cerebellar 
origin, for Horsley and Lowenthal showed that stimulation 
of the cerebellum in a decerebrate animal produced con¬ 
traction of biceps and active relaxation of triceps. The 
uniform structure of the cerebellum suggests uniform 
function; probably it is an organ which functions as a 
whole. Hughlings Jackson has always considered it to be 
an organ which presides over continuing movement, and 
therefore static functions, as distinct from the cerebrum, 
which initiates successive movements. 

Luciani’s experiments show that total removal produces 
parasthenia, or defective force, paratonia, or defective tone, 
and astasia, or unsteadiness of contraction. The cerebellum 
is connected with the opposite cerebral cortex, and with the 
mesencephalon; it is probably to the severence of the con¬ 
nections with the latter, in ablation of the organ, that 
may be attributed the disturbances in gait and station. 

In standing erect the cerebellum coordinates the inner¬ 
vation currents of the muscles of the limbs and trunk in 
such a way that the joints are fixed, and the line of the 
centre of gravity of the body passes through the knee- and 
ankle-joints. The weight of the body is therefore balanced 
upon the astragalus. This process is reflex and depends 
for its maintenance upon afferent impressions from the soles 
of the feet, and from the joints, muscles, and deep structures 
of the limbs and trunk, and from the semicircular canals. 


In walking the cerebellum is reflexly coordinating the 
innervation currents to the muscles of the resting leg, while 
the cerebral cortex is coordinating the successive movements 
of the advancing leg in progression. 


An ataxic, on closing his eyes, manifests instability of 
station—Romberg symptom. Normally, equable reflex 
spinal and cerebellar tonic contractions fix the jo’ints of the 
lower limbs, but when the afferent impressions from the 
deep structures of the limbs and from the soles of the feet 
are cut off by degeneration of the lumbo-sacral posterior 
roots, the ataxic patient has to rely upon impressions from 
the semicircular canals and visual sensations for the main¬ 
tenance of balance, by tonic contraction of opposing groups 
of muscles. When he closes his eyes, owing to the absence 
of guiding sensations he is unable to voluntarily reinforce 
by attention this tonic contraction ; consequently, the 
source of compensation for maintaining equilibrium is 
removed, and swaying takes place, which, by the sensation 
from the semicircular canals, warns him of his danger of 
falling by the change in his state of consciousness of 
position, enabling him to recover himself by attention and 
an effort of the will. Romberg’s symptom is an early 
phenomenon of tabes, and may exist without any cutaneous 
anaesthesia; it is due to the interruption of the subcortical 
reflex spinal and cerebellar circles by degeneration of those 
neurons with coarse fibres from deep structures, vide fig. 48. 

Before proceeding to discuss the mechanism of cortical 
coordination, it is necessary to make some observations 
concerning the efferent systems of neurons from cortex to 
muscle, by which voluntary reciprocal innervation takes 

The psycho-motor neurons lie in small groups in the 
cortex in a series corresponding to the segmental spinal 
series, except that the lowest occupy the top of the ascending 
frontal convolution; so that the longest axons arise from 
those cells which proceed to the lowest end of the cord 
(Sherrington.) These psycho-motor neurons become more 



complex the higher we rise in the zoological scale ; and the 
explanation is a proportional increase of combinations of 
association neurons which act directly upon an increased 
number of dendritic points of contact. Such cortical neurons 
are the effective agents of the will, regulating and adjusting 
by reciprocal innervation of spinal neurons the outgoing 
currents to muscles and the incoming currents connected 
with reflex muscular tonus. The diagram which has been 
used (fig. 48) is wrong in many respects; it represents, for 
simplicity, one psycho-motor neuron connected with one 
spinal motor neuron, whereas it is in indirect connection 
with many; otherwise the transection of the pyramids in the 
medulla should possess as many fibres as all the anterior 
roots put together. 

Yon Monakow is probably right in asserting that there is 
no direct connection between the psycho-motor neurons and 
the spinal motor neurons, but that intercalary neurons exist. 
Schafer has shown that the pyramidal fibres end at the base 
of the posterior horn and not in the anterior horns. Sherring¬ 
ton has, however, found degenerated fibres proceeding to the 
anterior horns. Von Monakow in his recent work gives the 
following paths of cortical impulses :— 

(1) A neuron, the axon of which enters the anterior horn 
and is brought into relation with groups of anterior horn- 
cells by means of an intervening intercalary neuron. 

(2) A neuron which ends in a terminal arborisation in the 
mescencephalon, and is brought into relation by an' inter¬ 
calary neuron with another neuron, the axon of which passes 
down the cord to end at the base of the posterior horn, and 
is thus brought into relationship with the terminal arborisa¬ 
tion of the afferent reflex spinal neurons, which again in¬ 
fluence the spinal motor neurons by an intervening inter¬ 
calary neuron. 

The experiments of Sherrington show that there is 
reciprocal innervation of functionally correlated groups of 
antagonist muscles, and we may assume that a group of 
psycho-motor neurons, when physiologically stimulated, initi¬ 
ates in the spinal gray matter innervation currents which 
augment the contraction in certain groups—for example, 


flexors—and inhibit the reflex tonus in the antagonists— 
for example, extensors. The adjustment of this reciprocal 
innervation determines the range, the rate, and the time of 
cessation of the movement; but subsidiary synergic groups 
of muscles nearly always co-operate, and are especially neces¬ 
sary in determining and maintaining the required direction 
of movement. Two paths from the cortex which Yon 
Monakow figures may therefore be the means of regulating 
this reciprocal innervation. Thus, if volition initiates a 
flexor movement, an impulse proceeds direct to the appro¬ 
priate flexor-motor neurons, and simultaneously an impulse 
flows to the spinal reflex anastomosis of the correlated 
extensor group, the result being increased innervation of 
the flexor group and inhibition of the tonus in the correlated 
extensor group. 

If, then, we are correct in assuming that there is a tract 
from the cortex which regulates and adjusts reflex tonus, we 
can understand that, as this reflex tonus is progressively 
abolished by the destruction of the posterior roots, there is 
a disturbance in the balance of reciprocal cortical innerva¬ 
tion of the spinal neurons, and the resulting incoordination 
is partly due to uncontrolled over-action of one system of 
cortical psycho-motor neurons. 

The physiological stimulus which excites, under the in¬ 
fluence of the will, appropriate groups of psycho-motor 
neurons for the regulation and adjustment of this reciprocal 
spinal innervation of synergic muscles, takes place at the 
synapses of their dendrites, with immediately correlated 
association neurons. Voluntary reinforcement of this 
stimulus may take place by attention, which is a concen¬ 
tration of consciousness, so that there is a partial with¬ 
drawal of physiological activity from the cortex as a whole, 
with a corresponding concentration in a particular system of 
neurons comprising sensory terminals and correlated groups 
of association neurons, the result being a more vivid revival 
in consciousness of tbe perception which precedes the move¬ 
ment willed. There is a sense of effort attending this 
process, which we may assume is associated with a using up 
of potential. 



After once the movement has been initiated, and repeated 
a number of times, the sense of effort becomes less and less, 
and it may be presumed that the nervous process is mainly 
subcortical after once the will has initiated the movement, 
and adjusted the necessary combinations of neurons for its 

In tabo-paralysis we have seen that a large proportion of 
the cases showed a degeneration of the crossed pyramidal 
tracts in the lumbo-sacral region, and we know that some of 
these cases showed very little ataxy in proportion to the 
degeneration, and a few exhibited less ataxy when the pro¬ 
cess of cortical degeneration occurred. The explanation 
may be that the long pyramidal fibres, having under¬ 
gone decay, do not now overact and upset the balance be¬ 
tween impulses going directly to the spinal motor neurons 
and those which influence reflex tonus. 

No doubt the cortex is continually sending impulses 
down the spinal cord inhibiting reflex tonus; and this 
probably accounts for the fact that the knee-jerk may 
come back after cortical injury or disease, also for the 
existence of the knee-jerk on one side and its absence on 
the other. When the knee-jerk is present it means that 
some of the posterior roots of the lumbar enlargement are 
still present to conduct impulses, though not enough to 
allow of sufficient reflex tonus to give the knee-jerk; unless 
by a progressive decay, or acute degenerative changes, the 
cortical inhibitory influence is withdrawn; then (as in 
Westphal’s experiments with strychnia), the knee-jerk is 
obtainable, because the afferent impressions now produce 
sufficient tonus. Jendrassik’s method of reinforcement is 
probably explained in the same way, for by grasping the 
hands and pulling, attention is concentrated in the arm area 
of the cortex, and there is a withdrawal of physiological 
activity from the leg area, therefore cerebral inhibition. 

The essential cause of locomotor ataxy is undoubtedly 
the degeneration of the posterior roots, but marked ataxy 
does not occur until there is some degeneration of the endo¬ 
genous systems. This may be due to the fact that muscle- 
tonus may be reflexly induced by efferent impressions coming 


from spinal segments other than those which are directly 
correlated with sensory and motor structures in which the 
posterior roots are completely degenerated. 

Further observations which I have made upon monkeys, 
in which the posterior roots have been divided by Professor 
Halliburton, have convinced me of two facts: (1) That 
a true ataxy of the upper limb cannot be produced by 
division of posterior roots, as Heriug has asserted; for 
either the animal showed no incoordination of move¬ 
ment ; or if, in cases when there was an insufficiency of 
roots divided to produce paralysis, there were jerky, inco¬ 
ordinate movements, they did not persist more than a few 
days; indeed, the animal which Hering quotes from 
Sherrington’s and my observations, as having shown inco¬ 
ordination, which it did only for a few days, was the one 
which we, some months later, showed at the Berne Physio¬ 
logical Congress, with complete sensory paralysis. 

Jules Soury, in an interesting summary of tabes, refers to 
the fact that Sherrington and I had shown sensory paralysis, 
but it was left to the sagacity of Hering to demonstrate the 
importance these experiments had upon the pathology of 
ataxy. This important relationship I had been fully aware 
of from the time that I made experimental sections of pos¬ 
terior roots in monkeys at the Brown Institution more than 
twelve years ago; but I have not yet satisfied myself that 
■section of posterior roots in animals can produce a condition 
similar to locomotor ataxy in man. Any incoordination of 
movement which may follow section of roots is either soon 
compensated, or followed by complete loss of voluntary 
ipower. We cannot produce that systemic, elective, and un¬ 
equal destruction of root fibres artificially. Ataxy is due, not 
only to loss of function from neuronic destruction, but to 
physiological over-action of structures, which normally act 
in opposition to those which are destroyed. 

One of the earliest paralytic signs of tabes is a loss of 
tonus in the dorsal flexors of the foot, and foot drop while the 
patient is lying on his back in bed (see Case 46). This may 
be partially due to gravity and the weight of the bed clothes. 
If the patient is told to flex his hip to the uttermost, it will 



be observed that the synergic dorsal flexion of the foot with 
hip and knee does not take place. By the aid of vision and 
attention he can produce the flexion, but it involves con¬ 
tinuous attention, and even then it is not synergic, but 
follows the hip-flexion. In walking the principal movement 
for progression is flexion of the hip, but the range of move¬ 
ment would be limited unless there was an associated 
flexion of the knee and dorsal flexion of the foot. 

Such a patient requires a stick or two sticks to widen his 
base of support, in order that he may so adjust his body that 
the line of the centre of gravity may fall within the basis of 
support, and that he may look at his feet and guide their 
movements. Thus, by cortical processes involving contin¬ 
uous attention he compensates for the failure of the normal 
kinsesthetic sensations which are associated with every suc¬ 
cessive movement, and which in all movements which habit 
or practice have made semi-autotnatic and periodic, become 
sub-conscious. Why, normally then, does the sense of a 
false movement immediately evoke consciousness of it ? 
Because volition, having determined the complexus of neu¬ 
rons to be employed in initiating a movement precise in 
range, rate, and direction, the successive combinations of 
neurons are by associative memory revived in orderly se¬ 
quence—the complexus of sensations in the last movement 
sufficing for the revival of the next in the series. 

Ingoing and outgoing currents are flowing through the 
cortical neurones without any expenditure of potential. A 
false step occasions a break in the lines of least resistance, 
with discharge of potential at the new arrival platform of 
kinsesthetic impressions. In both locomotor ataxy and 
general paralysis, there is a failure in coordination; but the 
cause is different; in the former, the coarse reflex and semi¬ 
automatic adjustments are at fault; in the latter, it is the fine 
cortical adjustment. In every conscious movement, both fine 
and coarse adjustment are used—the smaller the muscles, 
the more delicate are the minute alterations of their tensions, 
the greater and more varied is the complexity of their com¬ 
binations and adjustments. Complexity and multiplicity of 
movements determine the number of spinal motor neurons 



innervating groups of muscles, likewise the number and 
complexity of the communities and systems of neurons 
which precisely adjust the outflow of spinal innervation cur¬ 
rents to the muscles. Take as examples the association 
of the hand and the eye, the ear, and the motor speech 
apparatus in the performance of the specially endowed human 
faculties, the communication of ideas by visual or verbal 
symbols, which brings directly into play successive combina¬ 
tions of systems of neurons too complex to analyse, but 
involving directly a large part of the cerebral cortex, the 
mesencephalon and spinal axis. However, the muscles which 
are especially innervated form but a very small fraction of 
the whole mass. The fine cerebral adjustment of coordina¬ 
tion is continually and successively, by new combinations, 
infinite in number and variety, regulating the innervation 
currents of an infinite variety of spinal neurons, and thus 
adjusting the delicate tensions of correlated groups of minute 
muscles engaged in the expression of our thoughts and 
emotions. In general paralysis, the morbid process, early in 
the disease, strikes this fine adjustment in the cerebral 
cortex. The system of association neurons, which coordinate 
and associate the kinsesthetic impressions of near and dis¬ 
tant related ideation centres with the psycho-motor neurons, 
are in a state of progressive decay, and although there may 
be no disease of the efferent path from the cortex in the 
early stage of the disease, yet, owing to defective and un¬ 
equable stimulation of the cortical psycho-motor neurons, 
there is a failure in the precision of the reciprocal inner¬ 
vation of correlated groups of muscles used in verbal and 
written speech, manifest by tremor and incoordination. 
Some of the cases showed this very markedly, without pro¬ 
portional dementia and delusions. We must suppose that 
these were examples of functional selection in the morbid 

The Physiognomy. 

“ There is no art to find the mind’s construction in the 
face.” One of the earliest signs of general paralysis is 
afforded by the expression, and we may recognise broadly 



three types: (1) mask-like expression ; (2) exaltation; (3) de¬ 

The first denotes a blank mind without active delusions 
of exaltation or depression, but often considerable dementia. 
Every emotion has its muscular concomitant in individual 
expression, and Darwin showed that so intimate was the 
relation between the two, that attention directed in such 
a way as to evoke the motor response of a particular emotion 
was accompanied by the correlated feeling. 

In advanced dementia, the mind is a blank, there is 
absence of feeling, and consequently absence of motor 
response. Not only is there a blank expression in the face, 
but there is an expressionless hand. In those cases of the 
motor type, where there is lack of expression and marked 
speech affection without very much dementia, we may 
predict a more localised process (as in case 53) extensively 
destroying the neurons of association immediately connected 
with the psycho-motor neurons of the fronto-central regions. 
The conditions of exaltation and depression are, in all 
probability, partly due to neuronic destruction, partly to 
toxic and circulatory disturbances of the brain. The patho¬ 
logical process here acts like a magnifying glass, and control 
of what is passing in the mind no longer occurs. Like a 
muscular contracture in which one group of muscles con¬ 
tinually overpowers the other, although the innervation 
current of the more powerful group is less than the normal, 
yet its effect is continuous and apparently greater, because 
the innervation of its reciprocal antagonist group is very 
much less than the normal. 

The fixed ideas of exaltation or pain which we may 
coiisider as primary opposite emotional states, behave in the 
same way, and produce by the pathological process a magni¬ 
fied effect. 

A patient not infrequently presents an expression of 
mental pain and dejection, but grandiose delusions and exal¬ 
tation can be aroused in him by suggestion. The muscular 
concomitant is then shown by his facial expression; it im¬ 
mediately changes to one of exaltation, and the lustreless 
eye glistens when relating his wealth, strength, prowess or 



The emotions uncontrolled are reflected uncontrolled; and 
there is a failure in the reciprocal innervation of the muscles 
of expression owing to lack of reflex emotional tonus. 

The subject of coordination is one. of great interest, and I 
hope to deal more fully with its physiology and pathology 
in a future publication. 

Additional References not Contained in the Text. 

(1) *Redlich. “ Die Pathologie der tabischen Hinterstrangs Erkrankung,” 


(2) *Schmaus und Sacki. “ Vorlesungen fiber die Pathologischen Anatomie 

des Rficken marks ” (J. T. Bergmann, Wiesbaden, 1901). 

(3) *Furstner. “ Zur Pathologie und Pathologische Anatomie der Pro- 

gressiven Paralyse ins besondere iiber die Veranderungen des Rficken- 
marks und der peripheren Nerven.” Archiv. f. Pysch ., xxiv., 1893, 
ibid , “Ueber die spinalen Symptome bei der progressiven Paralyse,” 
Arch, f. Psych., Band xxxiii., Heft 3. 

(4) Gaupp. “Ueber die spinalen Symptome der progressiven Paralyse. 

Psychiatr. Abhandlungen herausgegeben von Wernicke, 1898.” 

(5) *Schmaus. “ Lubarsch und Ostertag Ergebnissen der Allgemeinen 

Pathologie. Rfickenmarksveranderungen bei progressiven Paralyse,” 
Jahrgang Abt. iii., p. 669. 

(6) Schmaus und Sacki, ibid. 5, Jahrg., p. 307. 

(7) Mendel’s “ Jahrberichte,” 1898-1901. 

(8) *Soury, J. “Anatomie et Physiologie pathologique du Tabes,” Revue 

Critique Archives de Neurologic, t. xi. et xii. 

(9) Nageotte. “ Tabes et Paralyse G4n4rale,” Th&se de Paris, 1893. 

(10) *Marie. “ Lemons sur les Maladies de la moelle epini&re,” Paris, 1892. 

(11) Philippe. “ Contribution a Tetude anatomique et clinique du Tabes 

dorsalis, ” Th&se de Paris, 1897. 

(12) Mott. “ Croonian Lectures : Degeneration of Neuron,” Lancet, 1900 ; 

“Archives of Neurology,” vol. i. 

(12a) Bruce and Muir. “On a Descending Degeneration in the Posterior 
Columns, &c.,” Brain , 1896. 

(13) *Dejerine et Theoari. “Contribution a l’etude des fibres 4 trajet 

descendant dans les cordons posterieurs de la moelle 4piniere,” 
Journal de Physiologie et de Pathologie gen. , Mars, 1899. 

(14) *Stewart, Purves. “ Degenerations following a Traumatic Lesion of 

the Spinal Cord in the Cervical Region,” Brain, 1901, No. 94, vol. xxiv. 

(15) Edinger. “ Eine neue Theorie iiber die Ursachen einiger Nervenkrank- 

heiten ins besondere der Neuritis und Tabes,” Volkmann's Samml. 
klin. Vortrag., N. F., Nr. 106, 1894; ibid., “Ueber experimentelle 
Erzeugung tabesartiger Riickenmarkskrankheiten,” Kongress f. innere 
Medicin in Wiesbaden, 1898. 


(16) Goldscheider. “ Ueber die Bedeutung der Reize f. Pathologie und 

Therapie in Licht der Neuronlehre. Kong. f. innere Medicin zu 
Liibeck,” 1897. 

(17) *Leyden-Goldscheider. “ Erkrankungen des Riickenmarks und der 

Medulla, ob.,” NothnageVs specielle Pathologie und Therapie , bd. x., 

(18) Gowers, Sir Wm. “ Diseases of the Nervous System.” 

(19) Transactions of the Pathol. Society , 1900. 

(20) *Head and Campbell. “The Pathology of Herpes Zoster,” Brain , 1900. 

(21) Dejerine. “ Semiologie du systeme nerveux,” Traite de Pathologic , 


(22) Uhtoff. “ Beitrage zu den Gesichtstauschungen bei Erkrankungen 

des Sehorgans,” Monatschrift fiir Psych, und Neurol. , 1899. 

(23) *Henschen. “ Klinische und anat. Beitrage zur Pathologie des Gehirns,” 

Upsala, 1890-94. 

(24) Ford Robertson. “ Pathology of Mental Diseases.” 

(25) Be van Lewis. “ Text-book of Mental Diseases.” 

(26) Alzheimer. “Beitrage zu pathologischen Anatomie der Hirnrinde,” 

Monatschrift fur Psych. Band ii. 

(27) Obersteiner. “Beitrage zu pathologischen Anatomie des Gehirnge- 

fasse,” Wiener Medicin. Jarhrbucher, 1877. 

(28) Marschalko. “ Ueber die sogenannten Plasmazellen, ein Beitrag zur 

Kentniss der Herkunft der Entziindlichen Infiltrationzellen,” 
Archiv. /. Dermat. und Syphilis, Bd. xxv. 

(29) *Vogt, Ragner. “Das Yorkommen von Plasmazellen in der Men- 

schlichen Hirnrinde, &c.,” Monatschrift fiir Psych. Band ix., 1901. 

(30) Mahaim. Bulletin de VAcadamie Roy ale de Medecine de Belgique, 

July, 1901. 

(31) Ha vet. “ Des lesions vasculaires du Csrveau dans la Paralyse Gene¬ 

rate,” Bulletin de VAcad . R. de Med., Belgique , July 26,1902. 

(32) Unna. “ Ueber eine Modification der Pappenheimschen Farbung auf 

Granoplasma und deren Anwendungsgebrauch,” Munchener Medicin- 
ische Wochenschrift, November 4, 1902. 

(33) Bulloch-Ehrlich and Madsden.* “A Review of Current Theories 

Regarding Immunity,” by James Ritchie, M.A., M.D.Oxon., Journal 
of Hygiene , vol. ii. 

34) * Welch. Huxley Lecture, “ Immunity,” Brit. Med . Journal , October, 

(35) Anderson, Hugh. Thesis for the Degree of M.D.Cantab. “The 

Medullation of Afferent Fibres.” 

(36) * Sherrington. Article, Spinal Cord. “ Text Book of Physiology,” 


(36a) Hughlings-Jackson. “The Central Nervous System,” Lancet , 1896. 

(37) ’Hering, H. E. “ Beitrage zur experimentellen Analyse coordinirter 

Bewegungen,” Separat. Abdruck aus dem. Archiv. fur die ges. 
Physiologic, Bd. 70. 


(38) *Fcerster Ottfrid. “ Die Pathologie der Coordination,” Verlag von 

Gustav Fischer, 1902. 

(39) ♦Von Monakow. “ Ueber den gegenwiirtigen Stand der Frage nach dei 

Lokalisation im Grosshirn,” Ergebnissc der Physiologie , BiophysiP 
und Psycliophysik , Bergmann, 1902. 

(40) Schafer. “ Essentials of Histology,” 1902. 

(41) Jendrassik. Deutches Archiv. fur Klin. Med., xliii. 1888. 

(42) Mott and Sherrington. “ Experiments upon the Influence of Sensory 

Nerves upon Movement and Nutrition of the Limbs.” Proceedings of 
the Royal Soc ., vol. lvii., 1895. 

(43) Bicker, Adolf. “ Ueber Einfluss der Sensiblen Nerven und der 

Labyrinthe auf die Bewegungen der Thiere.” Pfliiger's Archiv ., 
lxvii., 1897. 

♦ These works contain a very complete bibliography, and may be con¬ 
sulted for an analysis and summary of the conclusions arrived at by other 

%* I desire here to express my grateful obligations to my 
Colleagues at Charing Cross Hospital and to the Medical 
Superintendents and officers of the Asylums and Infirmaries 
for their kind assistance in calling my attention to the cases 
under their charge, and for permission to make observations 
and notes thereon. 




Late Technical Research Scholar of the London County Council. 


Section I.— The Causes of Amentia. —Introduction. Etiological Factors. 
General Considerations. 

Section II.— The Classification and Varieties of Amentia. —Primary 
Amentia. Secondary Amentia. Amentia with Epilepsy. Amentia with 
Paralysis. Amentia with Insanity. Table of Classification. 

Section III.— The Pathology of Amentia. —Notes on the Microscopical 
Examination of Twelve Cases. Tabulated Summary. 



Section I.— Etiology. 


In this paper are given the results of an attempt which 
has been made to ascertain the true causes underlying con¬ 
ditions of imperfect mental development, varying from gross 
idiocy on the one hand, to the mildest forms of imbecility 
on the other. Much as has been written on the subject, it 
is yet one of such great importance that it is hoped the 
account of a further investigation may prove to be not 
without value. 

The method which has been adopted is rather different 
to the usual one ; most of the previous work has been based 
upon statistics compiled from case books, in which way a 
very large amount of material is available, but the details 
are, unfortunately, so incomplete that the conclusions drawn 
from them are often far from satisfactory. In the present 
instance, therefore, the chief object has been to ensure as 
complete and accurate particulars as possible of the ante- 



cedents of every case by personal enquiries of the parents. 
In this way 150 satisfactory family histories have been 
obtained, in most cases embracing particulars of every 
member of the family for the last three generations, in a 
few the fourth is also included. In addition, the mental and 
physical states of the patients have also been carefully 
recorded, and noted from time to time for a period of nearly 
two years. 

The enquiry was at first confined to the patients within 
the London County asylums, but it was soon found that 
such did not include all the different types ; it was therefore 
extended, through the great kindness of the medical super¬ 
intendents, to the special institutions at Darenth and Earls- 
wood. In this way the writer had access to over 1,500 cases 
of various grades and types of amentia, and the complete 
histories of the 150 of these cases which have been obtained 
are thus representative of all the varieties of idiocy and 
imbecility which occur within the London area. This point 
is important, because the type of case varies much in the 
different institutions, and statistics which are confined to 
any one asylum cannot be considered as characteristic of 
the condition generally. 

It will be instructive to give some idea as to the preva¬ 
lence of these conditions. An accurate enumeration of the 
idiots and imbeciles in this or any other country is pro¬ 
bably impossible, but for practical purposes it may be 
estimated that in most civilised countries there is, on the 
average, one such to every 500 or 600 healthy persons. 
According to the recent census, the population of England 
and Wales is 32,525,716, and we shall not be far wrong in 
putting down the number of cases of amentia existing at 
the present time as 50,000. Shuttleworth calculated that 
in the year 1895 there were roughly about 42,000. .In 
France the returns a few years ago gave 36,000, but Bourne- 
ville, after a careful study of the subject, came to the con¬ 
clusion that this was far from accurate, and that the number 
was at least 60,000. In the United States in 1890 the 
official return of the number of such cases was 95,000, and 
this was generally considered to be an under-estimate. 



The above figures are sufficient to show the alarming 
extent to which idiocy and imbecility occur, and the impor¬ 
tance of carefully paying attention to the causes to which 
they are due. There is, however, a still further interest 
attaching to the subject of arrested or imperfect mental 
development. It will be shown that in the larger number 
of these cases there is a blight upon the embryo from the 
very beginning, and that its complete and perfect develop¬ 
ment is impossible ; also that this condition is more due 
to the seed than to the soil in which it grows, more due to 
the inherent condition of the germinal material than to 
the environment, important as the latter undoubtedly is. 
Idiocy indeed is, in most cases, the final expression of a 
tendency to degeneracy, which, first manifesting itself in 
deficient inhibitory power and instability of the nervous 
system, as is seen in hysteria and the like affections, passes, 
if unchecked, along its downward course, next revealing 
itself as epilepsy and various forms of insanity, to finally 
culminate in idiocy and the extinction of the family. Idiocy, 
therefore, is but the natural outcome of certain abnormal 
conditions of the germinal material, and in enquiring into 
its causes we are at the same time considering those factors 
which tend to bring about the general deterioration of the 

Before entering upon a detailed consideration of these 
various causes, it is necessary to briefly allude to a few 
points in the development of the normal brain. 

According to B. Boyd, the weight of the normal brain at 
birth is from 280-330 grams: during the first six months 
of life it increases to 600-680 grams, and at the age of one 
year it weighs about 750 grams; from this onward, growth 
proceeds somewhat more slowly until the weight of 1,300 
grams for the male, and 1,150 grams for the female is 
attained at the age of 12 to 14 years. A further slight 
increase takes place up to the age of 20 years, but after that 
further mental development, consisting in the perfection of 
the judgment, deliberation, and power of inhibition, takes 
place more by the elaboration of the association systems by 
which the complexity of nervous pathways is increased than 



by any marked increase in the weight of the brain. This 
elaboration is represented anatomically by a numerical 
increase in the fibres of the tangential systems (chiefly the 
outer line of Baillarger and the super and inter-radial fibres) 
and, according to the researches of Kaes, proceeds until the 
period of middle life is reached. After this age he states 
that a gradual diminution in these fibres takes place. They 
also undergo a marked atrophy in conditions of dementia, as 
I have myself verified by the microscopical examination of 
several such cases. The statement which has been made 
that the children of negro races in America are just as bright 
and capable of acquiring knowledge as the whites, up to the 
age of adolescence, but that they then rapidly fall behind, is 
very interesting in this connection. 

From these facts it follows that arrest of the development 
of the brain and consequent weak-mindedness may take place 
at any period up to middle life; practically, however, the 
term amentia is restricted to those cases in which this 
happens before the age of 12 or 14 years, but, as will be 
shown afterwards, it is rare for actual arrest of mental growth 
to be produced so late even as this, and more cases occur 
during the time when the most rapid increase in weight 
is taking place, i.e., before 2 years of age; the number of 
cases having their origin after birth at all, however, is com¬ 
paratively small, and an important point about these cases is 
that they are nearly always the result of a definite patho¬ 
logical lesion, which, in addition to the arrest of further 
growth, sooner or later brings about degeneration and con¬ 
sequent dementia. In the larger number of cases of amentia 
the development of the brain is not thus suddenly brought 
to a standstill, but the protoplasm set apart for the building 
up of the organ is from the very first incapable of proceeding 
to the perfect completion of the task, and a point is at length 
reached at which it can go no further; perhaps the term 
“ imperfect ” or “ incomplete ” development conveys a more 
accurate idea than “arrested ” as the latter rather suggests 
an external influence. 

It is most necessary to carefully distinguish between 
arrested or imperfect development (amentia), wad degeneration 



of already developed (it may be imperfectly) structures 
{dementia). Much confusion results from the extremely 
loose way in which the term “imbecile” is used; it should 1 
be restricted to the milder forms of amentia, but is very 
often wrongly applied to the milder forms of dementia 
following chronic insanity. 

That the two conditions of amentia and dementia 
gradually pass into one another is shown by some cases of 
adolescent insanity. In some of these it can be shown that 
in addition to the nervous instability, with its tendency to 
degeneration and dementia, there is also an incomplete 
development, or a mild degree of amentia. In such a high- 
grade imbecile the advent of adolescence or some slight 
exciting factor throws an increased strain upon a nervous 
system whose physiological margin is already very low, and 
an attack of insanity is the result; this constantly tends to 
recur, and eventually the signs of dementia appear. 

The two conditions may also occur simultaneously, as is 
strikingly shown in those imbeciles who develop general 
paralysis. Many of these cases have now been described, 
and such a condition was present in several of the writer’s 
cases. Another excellent example is seen in the dementia 
which supervenes in epileptic imbeciles. 

Having now cleared the way by defining generally the 
nature of the process, we can pass to a detailed account of 
the causes to which this arrest of development can be traced. 
It must be carefully borne in mind that many of these 
assigned “ causes ” are at best only contributing factors, 
indeed that some of them may be merely accidental circum¬ 
stances and have no connection whatever with the condition 
of the patient; in every instance we must guard against 
accepting as necessarily conclusive the explanation alleged 
by the parents. Our conception of these conditions will 
be more accurate if we look upon them as the result of 
several injurious influences, and not of any one individual 

These influences in their effects upon the developing 
embryo may be conveniently considered in the following 



(A) Intrinsic. 

The Condition of the Germinal Plasm. 

Under this heading come the following Hereditary Influences : 

(1) Insanity, &c. 

(2) Alcoholism. 

(3) Consumption. 

(4) Syphilis. 

(5) Consanguinity. 

(6) Old age or dissimilar age of parents. 

(B) Extrinsic. 

The Environment. 

1 (1) Abnormal conditions of the Mother during 

(a) Mental (worry, fright, shock, maternal 
impressions, illegitimacy, &c.) 

(b) Physical (alcoholism, presence of disease, 

(2) Injuries to the Fcetus. 

Abnormalities of labour. 

(a) Protracted. 

(6) Precipitate. 

4 (c) Instrumental. 

{d) Asphyxia neonatorum. 


^ Premature birth. 

(1) Traumatic. 

(2) Teething convulsions, epilepsy, &c. 

(3) Infectious fevers, &c. 

(4) Sunstroke. 

Etiological Factors.— (A) Causes Inherent in the 
Germinal Plasm. 

(Hereditary Influences.) 

(1) Abnormalities of the Nervous System (Insanity, 
Epilepsy, dkc.). 

It will be convenient to divide abnormalities of the 
nervous system into two groups, as follows :—1. Insanity, 
weakmindedness, and epilepsy. 2. Various other conditions, 
such as tendency to cerebral haemorrhages, paralyses, and 
definite neuroses not amounting to actual insanity. 

The following table shows the prevalence of these con¬ 
ditions in the 150 families examined :— 

Before Birth. 

During Birth. 

After Birth. 



Table 1. 

Showing the extent to ivhich Abnormal Conditions of the Nervous 
System were present. 

1.—Insanity, &c. 

2.—Other abnor¬ 

On the Paternal side only 

31*0 per cent. 

9*5 per cent. 

On the Maternal side only 



On both sides 



Total .. 

64-5 per cent. 

18*0 per cent. 

Grand Total. 82'5 per cent. 

The next table shows the extent to which this heredity 
existed in the direct and collateral lines respectively :—- 

Table 2. 

Occurrence of Insanity, <£c., in the Direct and Collateral Lines. 

1.—Insanity, &c. 

2.—Other abnor¬ 


In the Direct line only .. 

23*5 per cent. 

14*7 per cent. 

= 38 2 per cent. 

In the Collaterals only .. 



= 17 0 

In both Direct & Collaterals 

24*0 „ 

3*3 per cent. 

= 27-3 „ 


64*5 per cent. 

18*0 per cent. 

= 82*5 per cent. 

From these tables it is therefore seen that there is a 
definite history of abnormality of the nervous system in the 
antecedents of no less than 124 cases, or 82 - 5 per cent, of 
those examined, and that in 64 5 per cent, this is either 
insanity or epilepsy, and that in 65‘5 per cent, the abnor¬ 
mality occurs in the direct line. 

These figures are certainly very much higher than any 
previously obtained, a fact which I think is chiefly to be 
attributed to the thorough and searching enquiry which, in 
every instance, has been made into the patient’s antecedents. 


Until the printed enquiry form which is now so largely in 
use is discontinued, and its place taken by a personal 
investigation into the family history, we cannot hope to 
obtain satisfactory and reliable details upon which to base 
statistics of causation. I am glad • to say that such is 
now being done in some of the asylums. Dr. Taylor, 
the Medical Superintendent of Darenth Asylum, who has 
recently been making enquiries of this kind, tells me that 
he is becoming more and more convinced of the great 
importance of hereditary insanity, which he agrees with me 
in regarding as the chief factor in the production of idiocy. 

It may be as well to state that in the tables given above 
only those families have been included in which the predis¬ 
position was definite and undeniable; indeed, to give some 
idea as to the extent to which this occurred, the following 
facts may be cited:—Out of the 150 families examined, 
there were (including the patients) 420 individuals mentally 
affected. In addition there were 121 individuals who, 
though sane, had some marked abnormality of the nervous 
system like those which have been described; thus giving, 
on the average, 3 6 persons affected in each family. The 
greatest number of affected persons in one family was ten. 
Several of these cases demonstrate the existence in some 
families of a very distinct tendency to vascular lesions of the 
nervous system, especially haemorrhages. 

With regard to the particular kind of insanity from 
which these antecedents suffered, the information is too 
incomplete to admit of any satisfactory deductions. It is 
obvious that although evidence of the existence of insanity 
might be forthcoming, in many cases no reliance could be 
placed upon the informant’s account of its nature. In some 
instances, however, by searching through the case books of 
the asylums it has been possible to supply this, with the 
result that apparently the preceding insanity may be of any 
variety, and thus there are no grounds for thinking that one 
kind of mental disturbance more than another is liable in 
subsequent generations to be transformed into idiocy. Also 
the insanity in the parents need not necessarily have made 
its appearance before the birth of the patient. 



Referring again for a moment to Table No. 1, it is seen 
that the injurious influence is transmitted somewhat more 
often through the male than the female side. Yoisin, as a 
result of his researches, came to the opposite conclusion, and 
it is likely that if one had a sufficiently large series of cases 
there would be found to be no appreciable difference in this 
respect, and that the transmission occurred to about the 
same extent through the paternal and maternal sides. 

The question as to whether hereditary transmission is 
more likely to take place from one sex to the opposite or to 
the same one—that is, from father to daughter and from 
mother to son, or vice versa , is one which has been much 
discussed at different times. On such a matter pathological 
conditions like those now being considered, which can be 
readily traced, should throw some light. The following 
figures relate to this point:— 

In 61 cases in which the transmission was through the ) 34 were males. 

Father's side only j 27 ,, females 

In 39 cases in which the transmission was through the ) 23 were males. 

Mother's side only J 16 ,, females. 

In 24 cases in which the transmission was through both ) 12 were males. 

sides J 12 ,, females. 

From this it appears that the transmission occurs to 
about an equal extent to the same and to the opposite sex, 
although male children are more likely to be affected. 

(2) A Icoholism. 

Table 3. 

Showing the Number of Families in tvhich Alcoholism occurred. 


With insane 

With other 

Without any 
antecedent abnor¬ 
mality of nervous 
system, i 

On one side only 

26-0 per cent. 

65 per cent. 

4-5 per cent. 

On both sides .. .. \ 


4-5 „ 

1-5 „ 

3-5 „ 


30*5 per cent. 

8 0 per cent. 

8*0 per cent. 

Grand total of Alcoholism 


46 5 peTcent. 

1 In all these there was present either consumption in the ancestors, or 
some exciting cause in the environment of the patient. 


Alcoholism is therefore present in the antecedents in 
46"5 per cent, of cases, in the greater number in combination 
with insanity or other neuropathic conditions (38‘5 per cent.), 
in a very considerable number associated with consumption, 
and in only two • cases without either of these factors. In 
nearly all of those without neuropathic inheritance, however, 
there are other contributing causes, such as worry and ill- 
health of the mother during pregnancy, a severe attack of 
meningitis in the early months of life, &c. One way in 
which alcohol alone appears to be capable of occasionally 
producing idiocy will be alluded to under abnormal conditions 
of the mother during pregnancy. It will be seen that 
alcohol is rarely the sole cause of amentia, but on the other 
hand its importance as a contributing factor is very great; 
it will, perhaps, be better to draw attention to this after 
consumption has been considered. 

Certain authors, particularly the French, have attached 
great importance to the fact of the parents, especially the 
father, being under the influence of alcohol at the moment 
of conception. 

Quatrefages, Lucon, Morel, and,more recently, Boumeville 
have reported cases of idiocy which they considered due to 
this cause. The difficulty of obtaining reliable information 
of this kind is, of course, very great, on every possible 
occasion I tried to do so, and once thought that I had at 
last succeeded in getting definite confirmatory evidence. 
The informant was the mother of five children and she was 
perfectly certain that at the moment of conception of the 
patient, a pronounced idiot, the father was intoxicated. The 
case seemed clear, until further enquiry elicited the fact that 
a similar condition existed with regard to each of her other 
children, and these were well developed and healthy in every 
way. Since then I have obtained similar evidence in several 
other instances, the father being intoxicated at the concep¬ 
tion of the non-idiot as well as the idiot children, so that it 
cannot be said that my results afford any confirmation of 
this view. It is necessary to add that in each of the cases 
above mentioned careful enquiry revealed the presence of 
either insanity or consumption in addition to the alcoholic 



father; the probable reason why only one child was affected 
will be discussed later. 

Of course, many cases of alcoholism must in themselves 
be considered an undoubted evidence of a neuropathic taint, 
probably of a defective power of inhibition; this is suffi¬ 
ciently shown by the way in which, in some instances, the 
“ craving for drink ” may be passed on from generation to 

(3) Consumption. 

Under this heading are included in addition to pulmonary 
phthisis, caries of the spine, caseous glands, or any other 
undoubted tubercular lesion. 

Table 4. 

Showing the Number of Families in which Consumption occurred. 

With insane 

With other 

Without any 
antecedent abnor¬ 
mality of nervous 
system. 1 

On one side only .. 

16'0 per cent. 

6*0 per cent. 

5*5 per cent. 

On both sides . 

3-5 „ 

1-0 „ 

2-0 „ 


19 *5 per cent. 


7 *0 per cent. 

7'5 per cent. 

Grand Total of Consumption 

34*0 per cent. 

That is to say that in every 100 families in which weak- 
minded children are born, in thirty-four there exists a 
marked tendency to consumption or other tubercular lesions, 
which in the majority is also accompanied by some 
abnormality of the nervous system (generally insanity). If 
it were possible these figures should, of course, be compared 
with similar ones regarding the mentally normal population, 
but as far as I am aware, none such exist. From such 
particulars as I have been able to gather from hospital 
patients, however, I am convinced that although there is a 
large amount of consumption amongst the antecedents of 
the mentally sound, it is to nothing like this extent. Addi- 

1 In nine of these cases alcoholism was present in the ancestors in addition 
to the Phthisis; in the remaining two, although the Phthisis was strongly 
marked, I consider the amentia chiefly due to causes acting after birth, and 
these cases are, therefore, included in Table 7. 


tional evidence as to the presence of this diathesis is 
furnished by the large number of idiots and imbeciles who 
succumb to one form or other of tuberculosis. Ireland 
estimates this number at fully two-thirds of all cases. Of 
course, in many or even most of them the general deficiency 
of mental and physical vigour may increase their suscep¬ 
tibility to the action of the tubercle bacillus, but one cannot 
doubt that a very large number of these patients evince a 
very marked predisposition to the disease apart from this. 

With regard to the figures given under these two headings 
(alcohol and consumption) it must be clearly understood that 
the greatest possible care has been taken to include only 
those families in which their existence was well marked, as 
shown by there being at least three or four individuals 
affected in different generations of the family. Isolated 
examples have in no cases been counted unless occurring in 
the parents of the patient, and only then if very pronounced; 
otherwise the totals would have been very much greater 
than those given above. 

From what has already been said it will have been 
remarked that these three factors, nervous abnormality, 
alcoholism and phthisis, very frequently occur together in 
the same family. Their great importance in the causation 
of not only idiocy and imbecility, but also many other 
morbid conditions of the nervous system, as well as that 
general deterioration in the mental and physical health 
which is expressed by the term “ degeneracy,” it is, I 
believe, impossible to over-estimate. This subject will be 
referred to again later; for the present it will be enough to 
point out by means of the following table the extent to 
which these injurious influences occur in the same family. 

Table 5. 

Showing the occurrence of Insanity, Alcoholism and Consumption 
m the same Family. 

Alcohol occurred in .. .. .. 58 cases. 

Out of the 124 cases in Consumption occurred in .. .. 40 „ 

which Insanity or other _ Both Alcohol and Consumption 

abnormality of the nervous | occurred in.21 ,, 

system was present There was neither Alcohol nor Con¬ 
sumption in .. .. ..47 ,, 



( 4 ) Syphilis. 

In investigating the relation of syphilis to idiocy and 
imbecility, it must be kept in mind that even if it is certainly 
known that the father has suffered from this disease, if in 
addition a train of miscarriages and other signs indicate that 
the mother has been infected, or, lastly, even if the patient 
himself bears the undoubted marks of syphilis, it must not 
therefore be concluded that this is the cause of the arrest of 
mental development. That a normal condition of the 
nervous system is compatible with the presence of the 
syphilitic poison is apparent from a careful study of the 
many cases of congenital syphilis which may be seen in the 
out-patient department of any large hospital, and also from 
the not inconsiderable number of persons of mature age one 
constantly meets, who are marked with the well-known 
signs of inherited syphilis. Thus, although in a certain 
percentage of cases of amentia there are indications of the 
presence of this poison, the above facts would rather lead 
one to think that in such there must also exist some other 
factor. To give actual figures, out of the 150 cases 

Syphilis was certain in 4 (or 2 - 5 per cent.), the patients 
themselves presenting undoubted marks of the disease. 

Syphilis was possible in 5 (or 3 per cent.), a history of 
infection being obtained from the parents, although the 
patients showed no sign of the disease. 

Syphilis could not have been present, therefore, in more 
than 5'5 per cent, of cases, and probably not in so many, 
and in all of these there were other factors. The chief of 
these other causes was antecedent insanity which occurred 
in five of the cases; in the remainder there was either 
phthisis or alcohol, or both. 

The extent to which syphilis occurs amongst these 
patients is probably greater than amongst the mentally 
sound population, and its importance as a contributory 
factor must, I think, be admitted, but in view of the above 
figures, it seems to be only rarely that it can be looked 
upon as directly responsible for the patient’s mental 
condition. Here, as elsewhere, the great importance of 


hereditary neuropathic conditions is inevitably forced upon 
one, but where such exist I think the presence of syphilis 
is to be regarded as fraught with the gravest peril to the 
offspring. The syphilitic poison seems to have a special 
predilection for finding out the weak spot. 

The question as to whether syphilis alone is capable of 
producing idiocy is a most important one. In addition to 
the cases of which I have complete histories, I have had 
opportunities of examining over 1,000 idiots and imbeciles 
of varying grades at Darenth Asylums, and, including all 
these cases, I have only been able to discover four, or at 
most five, presenting signs of syphilis in whom careful 
enquiries failed to also reveal the existence of some other 
factor, generally insanity. 

There are two ways in which the syphilitic poison may 
act: in many instances it seems to have a powerful devita¬ 
lising action upon all the tissues of the body, bringing about 
changes of a degenerative nature, in fact, a premature 
decay; such may, perhaps, be considered as the remote 
effects of the virus. It is conceivable that the germinal 
material will share in this general lowering of vitality, and 
that the resulting offspring may, in consequence, be incapable 
of attaining perfect development; given at the same time 
neuropathic tendencies in addition to the syphilis, and the 
arrest will be liable to be specially marked upon the nervous 
system. This is the action of syphilis which has been con¬ 
sidered up to the present, and is the only action which can 
be looked upon as truly hereditary. 

On the other hand, in certain stages of the disease the 
toxic effects are much more marked, and a child born during 
this period is much more likely to possess the characteristic 
syphilitic lesions; the child is, indeed, suffering from the 
actual effects of the virus. The fault is in the environment, 
and not in the germinal plasm, and this action of syphilis 
should really be placed under the abnormal conditions of the 
mother during pregnancy except that it is more convenient 
to allude to it in this place. In the first group the idiot is a 
primary one {vide Classification), the morbid anatomy con¬ 
sists in an arrested development of the nerve-cells, and the 



condition is jiara-syphilitic. In the latter instance referred 
to, the patient comes into the secondary group, hereditary 
influences are not necessarily present, the morbid anatomy 
consists in one or other variety of “ brain syphilis,” to which 
the mental condition is secondary or symptomatic, and the 
condition is truly syphilitic. 

As a rule, there is not much difficulty in distinguishing 
between these two groups, and my opinion is that, in cases 
of amentia, the latter is decidedly more frequent; the cases 
usually show well-marked signs of a gross lesion (meningitis, 
softening, sclerosis, hydrocephalus, &c.), and the mental 
condition becomes progressively worse ; in fact, a condition 
of dementia soon supervenes. 

And here it may be noted that the effects of syphilis, in 
producing degeneration, are much more pronounced than in 
causing arrest. Its importance in the causation of general 
paralysis has already been fully shown by many authors, 
and, in striking confirmation of this from the entirely 
opposite point of view, is the fact that out of the cases here 
described in which syphilis was undoubtedly present, no less 
than three have since developed general paralysis in addition 
to the idiocy, as verified by post-mortem examination. 

It may be mentioned that even in regard to general 
paralysis occurring in adults evidence is accumulating to the 
effect that a neuropathic inheritance is also frequently 
present, and in the instances where this does not exist, it 
is still common to find that there has been some previous 
strain upon the nervous system, whereby the syphilitic 
poison has been enabled to get a hold. 

Dr. G. A. Sutherland, in his able paper on “ Mongolian 
Imbecility,” suggested that syphilis might be the cause of 
this variety of mental arrest. I have obtained complete 
family histories of several such cases, and have also examined 
many patients, but have been quite unable to find any 
confirmation of this theory. 

(5) Consanguinity. 

It is the general opinion that the intermarriage of blood 
relations is fraught with considerable evil effects, both 


mental and physical, to the offspring. That this is the case 
in certain of the domesticated animals there seems to be no 
doubt, and practically all breeders of experience are unani¬ 
mous that injury is almost certain to result from repeated 
“ in-breeding.” The effects upon the offspring are: the 
nervous system is rendered more excitable, and therefore 
more unstable, any existing constitutional defects are inten¬ 
sified, the size tends to decrease, and there is produced a 
predisposition to disease and an impairment of the repro¬ 
ductive functions. In other words, the result is a deterio¬ 
ration, and of exactly the same nature as that deterioration 
which takes place in the human being, the final expression 
of which is—idiocy. If, therefore, we can argue from the 
lower animals to man in this respect, and there is no reason 
for thinking that the laws governing reproduction are 
different in the two cases, consanguinity is undoubtedly 

That is to say, consanguinity carried on to the same 
extent as inbreeding in animals would be undoubtedly 
harmful; but practically such does not occur, and the two 
cases are not quite on the same footing. It is likely that if 
a regular system of intermarrying took place, the results 
would be most disastrous, and such a practice could not be 
too strongly condemned. The question of consanguinity, 
however, reduces itself for practical purposes into the occa¬ 
sional marrying of first cousins, and it is chiefly from this 
point of view that it has to be looked at. 

On the other hand, instances of repeated and systematic 
intermarrying, much more approaching to inbreeding in 
animals, are afforded by the Jews and the Quakers, also by 
the inhabitants of small out-of-the-way country districts 
and of inaccessible islands, cut off to a great extent from 
the rest of the world. It is an exceedingly difficult matter 
to obtain statistics of these peoples, and therefore to arrive 
at a definite conclusion on the subject. With regard to the 
Jews, however, there can be no doubt that as a race they 
are exceedingly neurotic and particularly prone to insanity 
and other diseases of the nervous system.. It is impossible 
in this place to cite actual figures in support of this state- 



ment, but much work on the subject has been done in 
different parts of Europe, and also lately in this country by 
Dr. C. F. Beadles, which fully endorses it. Still it must 
not be too readily assumed that consanguinity is necessarily 
responsible for all this. When one recalls the wretched 
conditions under which the Jews have been compelled to 
live for at least the past 2,000 years, from which, indeed, 
even now they are in many places not free, and when 
one thinks of the constant harrying to which they have all 
this time been subjected, it is not improbable that other 
factors than consanguinity may have left their mark upon 
the nervous system of the Jew. 

As to the Quakers, I have been unable to obtain any 
actual figures, but I have been assured by several people 
who have an intimate knowledge of them, that the pure 
Quakers are rapidly becoming extinct, and that insanity is 
very rife amongst them. 

Consanguinity to the degree in which it is practised by 
the Jews and Quakers must have injurious results, and if 
not the actual cause of deterioration must tend towards 
the propagation of defects which the introduction of new 
blood might dilute or even eradicate. In regard to the 
occasional marriage of first cousins, however, the case is 
different, and as a cause of idiocy I do not think this need be 
seriously thought of. Out of the 150 cases examined, such 
only occurred in seven instances, and in every one of these 
there were hereditary factors present, indeed in five of the 
cases there was well marked insanity. What is important 
to consider is the condition of the contracting persons : 
if these are in good health, and if their antecedents have 
been healthy and free from those diseases which have more 
particularly been found to give rise to deterioration in the 
descendents, then there is no objection to their marrying. 
I have known several instances of the marriage of first and 
second cousins without the slightest untoward result. From 
the practical point of view, therefore, the whole question 
turns upon this. 

Dr. Gillet, of Paris, in a paper recently published, 
comes to the conclusion that consanguinity plays a most 


important part in the production of idiocy, and at first sight 
his statistics seem to fully bear out his contention; but on 
a closer examination it is evident that he has completely 
ignored the question of the mental or physical condition of 
the ancestors, and simply taken note of the presence or 
absence of blood relationship. 

To sum up, whilst systematic intermarrying is decidedly 
injurious, the occasional marrying of blood relations, if both 
persons are in themselves healthy, and if they come of 
healthy stock, is not so. It is not, however, a practice to 
be advocated, being the means by which any existing 
defect (which would probably be present on both sides) 
would be accentuated in the offspring. 

(6) Old age of parents at birth of patient, or great 
dissimilarity in age of parents. 

It seems necessary to briefly allude to these factors as 
cases of idiocy are still not infrequently ascribed to them. 
Amongst the families examined, there were four in which 
a great dissimilarity existed in the ages of the parents, 
in all of them it was the father who was the elder, the 
greatest disparity being thirty-two years; in all of these 
cases, however, there was also present either insanity 
or well-marked neuropathic diathesis, in three of them 
accompanied by alcoholism, so that it is probable that 
the actual influence of these causes is really infinitesimal. 
I have made enquiries into several other cases in which 
similar differences of age existed without any neuropathic 
predisposition, and in these the offspring were perfectly 

(B) Causes Extrinsic to the Germinal Plasm. 


The individual factors of the environment may most 
conveniently be considered in the three stages before, during, 
and after birth. 

Those acting before birth are mostly referable to some 
abnormal mental or physical condition of the mother during 



pregnancy, although an actual injury to the foetus may also 
occur during this time. 

During birth they chiefly relate to the various abnormali¬ 
ties attending labour, and in this place reference will also be 
made to primogeniture and premature birth. After birth 
the factors are either traumatic, toxic, or some similiar 
morbid process, not yet fully understood. 

Factors acting before Birth. 

(1) A bnormal condition of the mother during pregnancy .— 
The unnatural condition of the mother may be either a 
mental or physical one, the former embraces worry, sudden 
fright or shock, and the much discussed subject of maternal 
impressions ; the bodily condition may be due to the presence 
of actual disease, or to a more general condition of imperfect 
health independent of any specific illness. The following 
table shows the extent to which these factors occurred in 
the cases examined :— 

Table 6. 

Abnormal Conditions of the Mother during Gestation. 

Hereditary Influences 

Present. 1 


f (a) Worry (illegitimacy of child, 


3*5 per cent. | 

Mental. - 

(6) Sudden fright or shock 

6-0 „ 


' (c) Maternal impression 



Physical. - 


' (d) Presence of actual disease 

( e ) General condition of ill-health 
k (insufficiency of food, &c.) 


*6 per cent. 

21-0 per cent. *6 per cent. 

"-- y -—-- 

Total .. .. .. 21*6 per cent. 

I have not mentioned insanity, consumption or alcoholism 
of long standing amongst these abnormal conditions of the 
mother, as they would rather tend to modify the germinal 


material and they have already been alluded to under heredi¬ 
tary influences. 

It is apparent from the above that a history of one of 
these causes is obtained in a very considerable number of 
cases, but careful enquiry shows that in nearly every instance 
there are also hereditary influences bringing about a deterio¬ 
ration of the germinal plasm entirely independently of these 
factors of the environment. It must not, however, be concluded 
that therefore they have no importance, for although the 
embryonic material may be healthy, its power of development 
is still in a certain measure dependent upon the quantity and 
quality of the nourishment supplied to it by the mother, and 
a condition of actual disease or extreme prostration during 
pregnancy cannot but be injurious to the growing ovum. 
In the cases in which the hereditary neuropathic predis¬ 
position to idiocy is but slight these external factors, indeed, 
appear to have an extremely important contributory influence, 
and they may make all the difference between a development 
of the nervous system compatible with the needs of every 
day life and one of mental deficiency; as will afterwards be 
referred to, these and similar contributory influences explain 
why it occasionally happens that an idiot may be born into 
a family of which the other members show no obvious mental 
or physical deterioration. 

The details which I have collected would tend to the view 
that in these cases the bodily condition of the mother is of 
more importance to the child than the mental state, and a 
condition of general physical prostration more often occurs 
than the presence of actual disease. In poorer people 
especially this malnutrition can often be directly traced to an 
insufficiency of food and fresh air during this critical time, 
due to the fact of the bread winner of the family being out 
of work; but apart from this it is perhaps scarcely to be 
wondered at that a large percentage of mothers in whom 
there is some hereditary taint should be very liable to evince 
mental or physical disturbances during pregnancy, which is 
a sufficiently trying period for women whose antecedents 
leave less to be desired. 

It is probable that frequently recurring pregnancies may 



also tend to bring about a diminished vitality of the mother 
and so contribute to the production of idiocy in cases where 
there exists a slight neuropathic predisposition; certainly 
the idiot child is often one of the later born in a large family, 
and especially is this so in the Mongolian type. 

Without entering into the vexed question of maternal 
impressions, it can be said that both these and the sudden 
frights and shocks which are often alleged to be the cause 
of the patient’s condition really have very little influence; 
so far I have been unable to discover a single case of this 
nature in which hereditary influences (commonly insanity) 
were not forthcoming upon a careful enquiry into the ante¬ 
cedents, so that whilst being unable to deny the possibility 
of idiocy resulting from such conditions, it can certainly 
be positively affirmed that such instances are exceedingly 
rare. It is not an uncommon event for a woman to give 
birth to a child during an attack of insanity, in fact a 
certain number of children are born every year actually 
within lunatic asylums, and I have elsewhere shown {vide 
Eef.) that their mental condition depends not upon the 
insanity of the mother, hut upon the presence or absence 
of morbid heredity; if the father is healthy and free from 
neuropathic taint, and the insanity of the mother is only 
of a transitory nature, the conditions are not yet ripe for 
the production of idiocy, which is the last stage on the 
downward path. 

There is one condition of the mother, however, which 
certainly does appear capable of producing idiocy in the 
absence of hereditary predisposition: this is excessive 
indulgence in alcohol. The following case appears to afford 
striking evidence to this effect: The father was a hard 
working industrious man, sound in body and mind, and 
coming of a healthy and long-lived family; he married the 
daughter of a small publican, apparently a healthy and 
happy girl, who used occasionally to serve behind the bar. 
Shortly after marriage this girl developed an insatiable 
craving for drink, all the money she could obtain by any 
pretence whatever, went in procuring it; later the ornaments 
and then the furniture of the house were pawned to feed her 



desires; ten months after marriage she gave birth to a. 
child—a hydrocephalic idiot, and according to the husband, 
she had scarcely known a sober moment during the preced¬ 
ing four or five months. Further enquiry showed that this 
woman’s father was also a heavy drinker, but otherwise 
there was an entire absence of any neuropathic condition in 
the family. Of course it may be that the alcoholic taste of 
the mother was in itself evidence of the neuropathic diathesis, 
but I cannot help thinking that the child’s condition was 
more largely due to an actual poisoning during its intra¬ 
uterine existence, and this view seems to be supported by 
the subsequent history, for the next child that was born, 
after an interval of nearly two years, was perfectly normal, 
and is now a bright and intelligent boy of 8 years; by 
this time, however, the mother had recovered, and had 
lived a perfectly steady life during the whole of the 

It is possible that occasionally other toxic conditions may 
bring about the same result, such, for instance, as the use of 
Ecbolics, and it is stated tjiat in America the use of these drugs 
is responsible for a considerable number of cases of feeble¬ 
mindedness ; syphilis may also act in the same way, as has 
already been mentioned; and some corroboration that the 
arrested development is actually due to the poison is fur¬ 
nished by the interesting series of experiments performed 
upon eggs by Fere; it must, however, be emphasised that 
cases of this nature are rare, and that in the large majority 
of idiots and imbeciles the presence of an abnormal condition 
of the mother during pregnancy has, at the most, only a 
contributing influence. 

(2) Injury .—In a few cases the patient’s condition is 
attributed to an injury received during its intra-uterine 
existence, but as these in no way differ from an injury after 
birth it will be better to refer to all the cases of trauma 

Factors acting during Birth. 

Abnormal labour .—It is generally considered that this 
is a very important and very frequent cause of idiocy. Beach 



and Shuttleworth attribute no less than 17 - 5 per cent, of 
their cases to such a condition; but my own observations 
emphatically tend to show that the importance of this 
factor as a cause of amentia has been much over-estimated, 
and that the number of cases really due to it is very small. 

The question is a most important one and beset with 
considerable difficulty; undoubtedly the extent to which 
abnormalities of labour will be found varies with the type of 
case examined. Thus I found such a condition to be much 
more frequent in the patients at Darenth Asylum than among 
those of the London County Asylums, the difference being 
due to the fact that cases in which there has been difficulty 
during birth are generally of the severest type owing to the 
arrest of development being complicated by an actual gross 
lesion, and they are, therefore, relegated to the special 

Out of the 150 cases examined some abnormality during 
labour was present in twenty-seven, or 18 per cent. The 
different kinds of abnormality were:—Precipitate labour, 2 per 
cent.; difficult and protracted labour with asphyxia neona¬ 
torum, 14 per cent.; with instrumental delivery, 2 per cent. 
But out of these twenty-seven cases there was a definite 
history of hereditary predisposition in no less than twenty- 
four, and in twenty-one of these actual insanity existed. 
The three cases in which no predisposition existed were 
cases of asphyxia neonatorum ; all are subject to epilepsy, 
to which the amentia is probably due. 

One seems justified in concluding from the above facts 
that mere difficulty during birth, even if attended with 
asphyxia, can only be looked upon as the actual and sole 
cause of the idiocy in a very small number of instances, 
probably not more than 1'5 per cent.; the parents of the 
patients, and especially the mothers, are, it is true, usually 
quite satisfied with the explanation they offer; but I am 
convinced that if more careful enquiries be made into all 
such cases hereditary influences will be found .to be present 
in a large number. 

It is probably true that difficulties during childbirth are 
more frequent when the child is weakminded than when it 


is healthy; but may not this be, in a certain measure, due 
to the very fact that the child is of defective nervous and 
bodily development, since the process of parturition probably 
depends to a certain extent upon the movements of a healthy 
and vigorous child ; and then again the mother who has an 
idiot for offspring is not unlikely herself to suffer from some 
deformity which presents more hindrance to labour than there 
would be in a perfectly healthy woman. 

Whilst, therefore, not admitting to this factor a very 
important part in the production of idiocy, it must be 
allowed that it may yet have a very considerable influence 
in aggravating the tendency to (or actually present) imper¬ 
fect development in the child; and certainly difficulties 
during labour, especially asphyxia, are in a great measure 
responsible for the gross brain lesions, with their resulting 
paralyses and convulsions, which occur in a large proportion 
of the more pronounced cases of amentia. 

Little, in an important paper published in the year 1862, 
was the first in this country to draw attention to the mental 
and physical defects resulting from abnormalities of labour. 
He collected a series of sixty-three cases presenting various 
defects of this kind, the most common abnormality being 
the presence of asphyxia due to protracted delivery ; but he 
himself says : “It is obvious that the great majority of 
stillborn infants whose lives are saved by the attendant 
accoucheur recover unharmed from that condition.” A state¬ 
ment which has since been fully endorsed by many eminent 
obstetricians, and which is confirmed by everyday experi¬ 
ence. It is indisputable that in a certain small percentage 
of cases in which asphyxia or other injurious factor is 
present some lesion of the brain results, causing a smaller 
or larger amount of paralysis—indeed, this condition is 
known as “Little’s disease,”—and that of these cases affected 
with paralysis a small number may also show mental 
impairment. Out of the sixty-three cases collected by 
Little, however, there were only eleven in which the intel¬ 
lect suffered, two of these being actually idiotic, and the 
remaining nine suffering from various degrees of feeble¬ 
mindedness, although in all his cases the patient was seen 



at an age at. which mental impairment would have been 
noticed had it existed ; indeed, the mental abilities of some 
of the other patients who were physically affected is 
described as being even beyond the average. Unfortu¬ 
nately, however, Little makes no mention of the family 
history in these cases, so that it is impossible to say 
whether there was or was not a neuropathic predisposition 
present in those children whose intellects suffered, and his 
paper, therefore, cannot be regarded as affording satisfactory 
evidence that amentia is at all a common result of abnor¬ 
malities of labour. 

If asphyxia leads to any evil result upon the nervous 
system, it does so by bringing about a vascular lesion 
(haemorrhage or thrombosis). It has been said, however, 
that arrested mental growth may be caused by actual com¬ 
pression of the brain tissue, in other words, by a species of 
trauma, and it is in this way that the use of forceps has 
been held responsible for some cases ; but when we consider 
the number of children who are daily delivered instru- 
mentally, and the fact that the head of the child is subjected 
to great alterations of shape during normal labour without 
any subsequent ill effects, it is clear that the unaided action 
of any of these factors in the production of idiocy must be 
very small, more particularly since, in the large majority of 
the cases in which such does occur, hereditary predisposition 
is also present. Further, artificial compression of the child’s 
bead after birth has been practised by several races of 
people, and is even still in use in the Toulouse district of 
France without any apparent evil effects, and certainly with¬ 
out producing idiocy. Spiegelberg says that “ the inden¬ 
tations and depressions which result in the cranial bones 
from pressure have a comparatively unimportant influence 
on the children.” It is also recorded of Samuel Johnson that 
he “ was born almost dead, and did not cry for some time.” 

Primogeniture .—It is said that first-bom children are 
more liable to suffer from amentia than those bom sub¬ 
sequently, and this is attributed partly to the more unstable 
mental condition of the mother during a first pregnancy, 
and partly to labour being more protracted in primipar® 


than in multipart. It has, however, already been seen that 
neither the mental state of the mother during gestation, nor 
the presence of difficulty during labour really have very much 
influence on the intellectual status of the child in the absence 
of neuropathic predisposition, so that it seems futile to 
seriously discuss the question of primogeniture. As a matter 
of fact, the statement that a large proportion of idiots are 
first-born children, is not beyond question. In the 150 
families examined, there were altogether 1,248 children, or 
an average of eight to each family; the proportion of first¬ 
borns is, therefore, as one to eight. Out of the total number 
of patients, there were sixteen first-borns, or a proportion of 
one to nine; from which it does not appear that there is a 
much greater incidence upon first-born than upon other 
children ; indeed, on the whole it seems to be more common 
for the idiot to be amongst the later-born, and very often he 
is actually the last child born alive in the family. In a 
family of degenerates, it is by no means unusual for the first 
one or two children to present no great departure from the 
normal; then come one or two who succumb to some ordin¬ 
ary ailment of childhood, from which a healthy child would 
probably have recovered, finally appears the idiot, and he 
is often followed by several children born dead. Of course, 
a sequence like this by no means invariably happens, but on 
the whole, in these degenerate families, there does certainly 
appear to be a tendency for each child to show more indica¬ 
tions of mental and physical deterioration than the one 
which has preceded it. 

Premature Birth .—7 per cent, of the patients were born 
prematurely, and in all of these hereditary predisposition \vas 
present. In cases where such is slight, it is possible that 
the alterations in nutrition brought about by the child being 
bom prematurely, may act as a determining factor in the 
way already described, but this is the extent to which 
premature birth is capable of affecting the mental condition 
of the child. 

Factors Acting after Birth. 

The factors acting after birth which are said to produce, 
or to be concerned in the production of amentia embrace 



trauma, epilepsy, teething convulsions, sunstroke, infectious 
diseases and similar morbid processes. 

It is rare for any one of these, unaided, to give rise to 
amentia, and although the actual pathological process present 
may vary with the cause of its production, in by far the 
majority of cases, its influence in bringing about arrested 
development is purely contributory; in a few cases, however 
(5'5 per cent.), there is no hereditary predisposition, at all 
events none can be ascertained, and the resulting imbecility 
appears to be due to one of these factors; even in these, 
however, the immediate result of the lesion is nearly always 
epilepsy, and it is to the constant recurrence of severe fits, 
that the arrested mental growth is due. 

The following table shows the extent to which these 
factors occurred:— 

Table 7. 

Showing the Factors acting After Birth. 



Without neuropathic 


by Epilepsy. 

No Epilepsy. 

(1) Epilepsy (Idiopathic) .. 

i 9 cases. 

3 ! cases. 


(2) Teething Convulsions 

8 „ 

2* „ 


(3) Infectious Fever and similar 
“ Toxic ” Influences 

5 „ 

l 3 case. 

I 4 case. 

(4) Trauma . 

5 „ 

I 4 

x ji 


(5) Sunstroke . 



I 7 case. 

27 cases or 

8 cases or 

2 cases or 

18-0 % 


_ lf% 

Totals .. 



1. (a) Both maternal and paternal grandfather died suddenly at an early 
age also well-marked phthisis on one side. 

(b) Mild amentia resulting from epilepsy said to have been produced by 
overstudy at school. 


(c) Mild amentia resulting from epilepsy due to patient having been 
nearly drowned. 

2. (a) Fits ceased after teething and reappeared at age of 6 years, since 
when they have persisted. A typical case of epilepsy with only slight 
amentia. The father used to be alcoholic, and his father appears to have 
been decidedly neurotic. 

(6) Well-marked phthisis on the mother’s side. A mild degree of amentia 
accompanying epilepsy. 

3. Fits following whooping-cough at the age of 6 months. Strongly 
marked phthisis on mother’s side. 

4. Slight amentia with gradually progressing dementia following enteric at 
age of eight years. No other cause discoverable. 

5. Severe fall on to stone pavement at age of 4 years; unconscious for a long 
time—a week afterwards severe convulsions—very frequent and severe fits 
since. Pronounced amentia with much dementia. No other cause discover¬ 
able than fall. 

6. Fits from 8 months, after sunstroke. Pronounced epileptic with con¬ 
siderable amentia and slight dementia. No other cause. 

7. Sunstroke in India, age 8 years. No other cause. A condition of mild 
imbecility without epilepsy. 

(1) Epilepsy {Idiopathic). —The number of cases of amen¬ 
tia which are the result of epilepsy occurring in early life is 
by no means inconsiderable, being probably about 10 per cent. 
The subject will be again referred to under the next heading, 
but it may be stated here that although the condition is 
perhaps more analogous to dementia, the fact of the disease 
appearing before the age at which much mental growth has 
taken place necessarily produces an arrest of development as 
well—in other words a state of true secondary amentia. In 
by far the greater number of cases the epilepsy is brought 
about by hereditary influences, but the disease, having made 
its appearance, must be considered as one of the factors 
acting after birth. 

(2) Teething Convulsions. —Convulsions occurring during 
the first dentition are often alleged as the cause of idiocy, 
but when one considers that a very large number of children 
have severe fits at this time and yet show no subsequent 
mental impairment, it is obvious that this condition by itself 
cannot play a very important part in producing amentia. It 
is conceivable that in severe and prolonged convulsions a 
small haemorrhage may take place and an actual lesion of 
the brain be produced, but the brain of a healthy child in 
most cases appears capable of recovering even from this. 



Out of the ten cases in which the patients’ condition was 
attributed to this factor there existed well marked hereditary 
influences (insanity or other abnormality of the nervous 
system) in eight, and it seems likely that in these the 
convulsions were but the manifestation of that same pre¬ 
disposition, in many of them being one of the earliest 
symptoms forthcoming of the presence of actual amentia ; in 
a few, indeed, the mother had noticed that the child was not 
quite bright and like other children before the fits. 

On the other hand, in several instances the teething con¬ 
vulsions are but the first indication of ordinary idiopathic 
epilepsy, and it is to the persistence of this that the mental 
arrest is due. Gowers states that “ a considerable number 
of cases of epilepsy date from infantile convulsions,” not 
that dentition is actually the cause of the epilepsy, but it 
supplies the necessary excitation to an already present pre¬ 
disposition. On the whole my observations would certainly 
appear to show that “ eclampsic idiocy,” that is, idiocy due 
solely to teething convulsions, in the absence of neuropathic 
inheritance is decidly rare, and that in the great majority of 
cases in which mental impairment is afterwards noticed the 
convulsions have either been the first symptom of that con¬ 
dition and not the cause, or else have been the first indication 
of the presence of idiopathic epilepsy ; of course, if epilepsy 
make its appearance at such an early period in the child’s 
life, and if it persist, arrest of intellectual development is 
almost certain to take place, followed later by dementia. 
Here, however, it is epilepsy that is the primary disorder, and 
the condition is one closely resembling epileptic dementia, 
with the addition that more or loss complete arrest has also 
been produced owing to the early onset of the attacks. 
(Vide “Amentia with Epilepsy,” Section H.). 

(3) Infectious Fevers, dc .—In certain acute infectious 
diseases occurring in early childhood such as scarlet fever, 
enteric, whooping cough, diphtheria, otitis, rhinitis, and also 
in some cases of meningitis, there are indications that a lesion 
of the central nervous system has been produced, probably 
owing to embolism, thrombosis or haemorrhage. In another 
type of case the disease appears closely to resemble acute 


anterior polio-myelitis and has been named by Striimpell 
“ acute polio-encephalitis.” As a result of these conditions 
various forms of paralyses frequently occur, and also convul¬ 
sions, which at first have a localised character but afterwards 
become general and closely resemble idiopathic epilepsy. 
Retardation of mental development is a not uncommon 
accompaniment of such conditions ; but cases in which they 
give rise to definite amentia in the absence of neuropathic 
predisposition or frequently recurring convulsive attacks are 
exceedingly rare ; indeed, I have only met with one such 

It is probable that the form of idiocy known as “ infantile 
cerebral degeneration” or “amaurotic family idiocy” is 
really due to some form of toxine, although the pathology 
of this disease is still very obscure ; the condition, however, 
is more one of a progressive degeneration than of amentia, 
although, of course, incidentally arrest of development also 

(4) Trauma .—In a certain proportion of cases the patient’s 
condition is attributed to a direct injury to the head at an 
early period of life, most commonly a fall. Sometimes the 
injury is said to have been inflicted upon the pregnant 
uterus, and at others compression of the head by forceps is 
held responsible. 

In the larger number of cases of this description a careful 
enquiry into the nature of the alleged trauma is sufficient to 
show its triviality, and to demonstrate that it could have 
had no connection with the subsequent mental condition of 
the patient; indeed, in all these cases of slight injury which 
I have examined there exists a well-marked hereditary pre¬ 

In the cases of severe injury, however, it occasionally 
happens that the most searching enquiry fails to reveal any 
factor whatever except the injury. This occurred in but one 
of the cases examined, in which the patient fell from a 
height of about three feet on to a stone pavement, alighting 
upon her head. Considering that in this case the family 
history is a fairly good one on both sides, and that the 
patient has eleven brothers and sisters all apparently in the 



best of bodily and mental health, the connection between 
the injury and the resulting mental impairment appears to 
be clear. The patient was unconscious for a long time after 
the accident, and about a week later had a series of severe 
convulsions. These have continued on and off ever since, 
and at the present time are indistinguishable from ordinary 
epilepsy; scarcely a day passes without an attack, and some 
days there are two or three severe ones. In this case I 
think the condition is really more of the nature of traumatic 
epilepsy, and that the unexpanded intellect is due to the 
nerve storms which have been almost constantly present from 
the age of three years. 

Between the two extreme degrees of injury above described 
there is a small number of cases in which the trauma seems 
to play the part of an exciting factor. It is rarely as severe 
as in the case just alluded to, but the condition of the child 
following the accident undoubtedly points to the presence of 
a lesion of the brain, generally of the nature of a haemor¬ 
rhage or laceration of brain tissue. In all the instances of 
this kind hereditary predisposition was present, and most 
probably it is owing to this that the development of the 
uninjured portion of the brain cannot take place sufficiently 
to compensate for that rendered useless by the trauma. 
Where epilepsy supervenes we probably have a constantly 
spreading pathological process against which no amount of 
compensation would avail. This question of compensation 
will be discussed more fully later; but it may here be 
remarked that head injuries of quite as severe a nature as 
those above referred to are by no means uncommon in 
children, and yet it is extremely rare for them to be followed 
by any permanent mental deterioration. 

(5) Sunstroke .—In two instances the condition of the 
patient was ascribed to sunstroke, one occurring in India, 
and the other in this country during a very hot summer. 
In each case the child had previously seemed quite well, and 
the attack was immediately followed by a lengthy illness 
apparently of the nature of meningitis. The family history 
was good, and no other cause discoverable than the one 
alleged. It would therefore appear that in a small per- 



centage of cases sunstroke may actually produce amentia. 
In one of the above there is only present a mild degree of 
imbecility, in the other the illness was almost immediately 
followed by severe convulsions, and the patient is now a 
typical epileptic, so that the arrested development is most 
likely the result of the fits. I have not yet had an oppor¬ 
tunity of making a post-mortem, examination of any similar 
case, but presumably the condition is one of meningo¬ 
encephalitis or of vascular alterations similar to those brought 
about by toxic influences. 

Rickets .—It is unnecessary to seriously consider the 
question of rickets as a cause of amentia, although some 
writers seem to think this disease can so act, and even speak 
of “ rachitic idiocy.” Undoubtedly rickets occurs in idiots 
and imbeciles, whether to a greater extent than amongst 
mentally healthy children I do not know; certainly, how¬ 
ever, the association of rickets and amentia is not strik¬ 
ingly common, and even if it were, it would surely be more 
rational to consider the rickets the outcome of the general 
mental and bodily degeneracy than its cause. 

. Sex .—It is a somewhat singular fact that whilst the 
various forms of insanity are more frequent in the female 
than in the male sex, the reverse is the case with amentia. 
Upon this main point all writers are agreed, although the 
relative proportion existing has been variously stated. From 
German statistics Piper comes to the conclusion that there 
are two males to one female, but from my own observations 
upon cases in this country, as well as from statistics 
obtained from many asylums, the incidence on the male sex 
would not appear to be quite so high, and, speaking gener¬ 
ally of all the varieties of amentia, I should say that the 
number is in the proportion of three males to two females. 

The following tabulated form gives the ascertained 
factors to which it is considered the amentia is due in the 
cases investigated; it is therefore a very condensed sum¬ 
mary of the preceding pages. 



I.—Hereditary Influences. 

. .. T | 97 cases or 

(A) Insanity or Epilepsy \ 64 . 5 per cent 

Other Abnormalities f 27 cases or 
of the Nervous System l 18*0 per cent. 

In 58 cases or 38*5 per cent, alcoholism was also present. 

In 40 „ 

26-5 „ 


In 21 „ 

14-0 „ 


In 4 

2-5 „ 


(Z?) Both Phthisis and Alcoholism (without neuropathic inheri¬ 
tance) .. .. .. .. .. .. .. .. 9 .. 6 0 

(C) Alcoholism .. .. .. .. .. .. .. .. 2 .. 1*5 

Case I.—Both parents drunkards, mother immoral, dis¬ 
solute and criminal. 

Case II.—Father drunkard, patient an epileptic with 
mild dementia. 

Total of Primary Amentia .. 135 .. 90 0 

Cases. cen ^ a g e# 

Total neuropathic 
inheritance .. 124 .. 82*5 

II.—Extrinsic Causes. 

(D) Before Birth. Abnormal condition of mother during 

Case I.—Mother alcoholic during whole of pregnancy. 
Case II.—Patient has well marked congenital syphilis, 
there is also a strong family history of 

(E) During Birth. Asphyxia Neonatorum 

In all cases epileptic fits have persisted from a very early 
age, to which the amentia is probably due. 

2 .. 13 

3 .. 2 *0 


After Birth. 4 

r Epilepsy and teething convulsions . 

. 5 cases' 


• 1 „ 


• 2 „ 

Toxic process .. 

• 2 „ / 



Total of Secondary Amentia .. .. 15 .. 10*0 

From this summary it will be seen that 90 per cent, are 
cases of primary amentia, being due to hereditary influences ; 
whilst 10 per cent, are cases of secondary amentia, being due 
to extrinsic causes ; but of these latter there are only 
6 per cent, which may be looked upon as the result of 
unavoidable causes (see notes to Table 7), and in 5 per 
cent, of these the amentia was accompanied by, and prob¬ 
ably due to, epileptic convulsions. 



General Considerations. 

Having now given an account of the various etiological 
factors which have come to light in the course of this inves¬ 
tigation, and pointed out their importance or otherwise, as 
well as the extent to which they occur, it becomes necessary 
to consider the manner in which they act in producing 

At the outset it is essential that we should carefully 
bear in mind what amentia really is. Generally speaking, 
its various grades are not to be looked upon as due to the 
presence of a definite disease or morbid process super-added 
to, or incident upon, a normal nervous system. There are, 
it is true, a small number of cases in which arrested mental 
development is the incidental accompaniment of some such 
pathological condition, the tendency being to dementia, and 
the entire process one of degeneration. The number of 
these cases, however, is small, and clinical experience and 
pathological research show that in by far the larger number 
of cases of amentia the prime condition is one of imperfect 
or incomplete development; in other words, a pronounced 
falling short of the standard normally attained. In the 
higher types of imbecility this imperfect development has 
fallen exclusively upon the central nervous system, and more 
particularly upon the higher portions of the brain, but in the 
more gross forms of idiocy many other parts of the organism 
are involved in the same incompleteness, as is amply shown 
by the general physical condition of such patients. Our 
conception of amentia, therefore, is not that of a definite 
disease, but of a developmental failure of either slight or 
pronounced degree. 

It is in this respect that amentia differs from insanity. 
In most cases of the latter affection the condition may be 
regarded as one of premature degeneration of certain por¬ 
tions of tbe nervous system which have attained normal 
development, this degeneration in most instances being the 
result of hereditary influences, whilst in others it may be 
brought about by the action of “ toxines ” ; but the gradual 
process of' decay gives rise to various abnormal mental 



states which we designate insanity, until finally more or less 
complete degeneration and dementia result. 

We have now to study the manner in which this failure 
of development, which is the anatomical basis of amentia, is 
brought about. It has already been seen that the etiological 
factors are divisible into two groups, viz.:—I. Hereditary 
Influences (or factors in the environment of the ancestors); 
2. External Influences (or factors in the environment of the 
patient ); and these two groups must be considered separately. 

Group I.—Hereditary Influences. 

It would obviously be out of place to enter into any 
detailed discussion of the various theories which have been 
advanced regarding heredity; there are some points, how¬ 
ever, which have a direct bearing upon the subject of 
amentia, and which must, therefore, be referred to. The 
views advanced by Weismann fully demonstrate the import¬ 
ance of the germ plasm in the transmission of qualities from 
parent to offspring, and in this respect are of great value ; 
but it seems to me that everyday medical experience is very 
much at variance with his view that this germ plasm is not, 
or is only to a very small extent, influenced by the environ¬ 
ment—that is by abnormal conditions of life, and more 
particularly by the presence of disease, which apparently is 
his contention. With regard to the transmission of acquired 
qualities which only affect the somatoplasm, the evidence is 
certainly negative, and as far as I am aware there are no 
recorded instances of the transmission of mutilations (even 
when performed systematically and upon many generations, 
as in the case of circumcision), or of the transmission of 
actual disease except where the embryo was directly affected 
by means of the placental blood. Amentia, however, does 
not come into this category, nor, for the matter of that, 
do such diseases as insanity or consumption; and it is not 
conceived that this is the way in which the sins of the 
fathers are visited upon the children even to the third and 
fourth generations. In the conditions j ust referred to it is not 
contended that the actual diseases are transmitted, but that, 
owing to their presence in the ascendant, the germ plasm 



has become so modified that the resulting offspring is 
rendered peculiarly susceptible to the action of certain 
influences; in other words, there exists what is commonly 
called a “ diathesis.” Similarly in amentia : what is trans¬ 
mitted is germinal plasm of such a peculiarly modified 
nature that the development from it of a complete, perfect, 
and healthy human being is impossible. We cannot doubt 
that this peculiarity of germ plasm exists; what, then, is 
the cause ? 

The morbid conditions which have been described as 
occurring in the ancestors of these cases of amentia are 
present in such a large proportion of cases that it would 
surely be quite unreasonable to imagine that they bore no 
relation to the resulting imperfect development. It cannot 
be looked upon as a chance coincidence that out of 100 cases 
of amentia, abnormalities of the nervous system (chiefly 
insanity or epilepsy) should be present in the ancestors of 
more than eighty, and alcoholism and consumption in forty- 
seven and thirty-four respectively; and yet this would 
appear to be the contention of Weismann, if he believes that 
the germ plasm is practically incapable of modification by 
its environment. 

I imagine that, at any rate, no one will deny that the 
tissues and organs of the body—the somatoplasm—may be 
altered in the individual by external influences, and par¬ 
ticularly by the presence of disease, such, for instance, as 
consumption and alcoholism; or will do other than agree 
that the immunity which follows certain of the infectious 
diseases is the result of some similar change. For our 
present purpose the diseases which affect the human body 
may be divided into two kinds; on the one hand are those 
in which the morbid process is practically confined to one 
organ and is chiefly local in its effects, or if general is of 
only a transitory nature; such diseases may be compared to 
mutilations and abnormalities of the somatoplasm, and their 
effect on the germ plasm is probably nil. On the other 
hand, however, there are certain diseases and morbid 
influences which bring about a profound change in many, if 
not all, of the organs and tissues of the body, either, it may 



be, by a direct poisonous action, or by causing pronounced 
alterations of nutrition. Among this class are consumption, 
syphilis, and alcoholism. Whether the action of such factors 
is directly toxic in nature, or whether they interfere with 
the general nutrition of the body, is no great matter; daily 
clinical experience and post-mortem examination amply show 
that there is present a great and almost universal pathological 
change. Is it conceivable that amid all this change the 
germinal plasm should remain entirely unaffected ? 

It is on this point that I believe the experience of the 
physician who has daily opportunities of observing the 
differences which exist between the descendants of such 
diseased individuals and those of healthy ones is strikingly 
opposed to this hypothesis of Weismann, and one sees so 
many instances in daily medical practice of a weakly and 
puny offspring of these patients, who seems “ born to trouble 
as the sparks fly upward,” that it is impossible to avoid the 
conclusion that some modification of the germ plasm has 
taken place. Further, the important work of Fournier in 
connection with syphilis gives additional support to such a 
view. He has fully shown by many cases that the syphilitic 
virus is capable of producing many and varied pathological 
changes in the offspring of the affected parent. I do not 
refer to those which are the result of a direct infection 
through the placental blood, but to the “ parasyphilitic ” 
conditions, which seem to be only capable of explanation on 
the view that some alteration in the germ plasm has been 
brought about. 

For my own part I do not see any other reasonable 
construction which can be put upon the figures given in the 
preceding tables than that the presence of these morbid 
conditions in the ancestors has so modified the germ plasm, 
either by direct toxic action or by interfering with its 
nutrition and vitality, that it is incapable of producing a 
perfectly developed being; indeed, I would go even further 
and say that the subject of amentia and the data which 
have been collected in this investigation afford very definite 
evidence that such really does take place; and that it is by 
reason of such modifications in an unfavourable direction 



that disease is perpetuated, and it is owing to the inherent 
capabilities of the germ plasm for such modification that 
evolution is a fact and the future advancement of the race a 
possibility. Let us, then, away with this fatalism, and 
remember that each individual is a potent factor which must 
operate either for the advancement or the retrogression of 
the generations to come. An idiot is no freak of Nature or 
haphazard gift of Providence ; in Nature there are no freaks, 
and idiocy and imbecility are but the outcome of the action 
of definite laws. 

It has been already stated that amentia is a condition of 
imperfect development, it is also the final expression of a 
progressive neuropathic degeneration, and in many of the 
histories which I have collected it is possible to trace this 
downward march. From family histories taken of cases in 
the different grades of this neuropathic degeneration it is 
found that well-marked abnormalities of the nervous system 
in the ancestors exist to a far greater extent in amentia 
than in any of the other grades; next to this they occur 
most frequently in insanity and epilepsy (especially the 
more severe forms which tend to result in rapid dementia) ; 
and they are relatively infrequent in the milder forms of 
epilepsy, hysteria, and neuralgia. In a very large number of 
the latter affections, however, there is present a history of 
alcoholism or consumption, very often both, and I believe 
that these two conditions play a most important part in the 
origination of the neuropathic diathesis. Idiocy, then, is the 
final expression of a neuropathic tendency, the earliest 
manifestations of which are hysteria, chronic neuralgia, and 
the minor forms of epilepsy; in the next stage appear more 
severe epilepsy, (usually dating from an earlier period of life) 
insanity, and tendency to early dementia; and last of all 
idiocy, with obvious evidences of physical degeneracy and 
very often extinction of the family. The most reasonable 
view would seem to be that the germinal plasm shares in the 
general bodily deterioration which results from the harmful 
conditions mentioned above, and that, therefore, the offspring 
to which it gives rise is rendered unstable and of diminished 
vital energy in the most delicate and newly acquired portion 



of its complex organisation—the nervous system—in other 
words, a neuropath has been created ; should such a person 
marry another with similar neuropathic tendencies an 
aggravation of the condition will be the result in the next 
generation, and epilepsy and actual insanity will probably be 
present. If a repetition of the same process occurs marked 
degeneracy will be present in the third generation with a 
strong probability that one or more members will be actual 
idiots or imbeciles. 

Of course, there are probably other factors besides 
alcoholism and consumption which contribute to this first 
departure from the normal, but which, being less marked, 
are not so capable of recognition. It is indeed more than 
likely that many of the conditions of life at the present 
day, the struggle for place or for mere existence, with its 
accompanying wear and tear and nervous strain, and often 
insufficiency of food and fresh air, contribute largely not only 
to the deterioration of our manners but also of our nervous 
systems, and tend to initiate that neuropathic diathesis, that 
slight departure from the nervous normal, which, if un¬ 
checked, will pass on to epilepsy, to insanity, and finally to 

It is not, of course, intended that the three grades of 
mental affection above described are necessarily restricted to 
three consecutive generations. All the varieties may, and 
frequently do, exist among the members of one generation, 
and it even occasionally happens that idiocy of the grossest 
type results from the presence of alcoholism and consump¬ 
tion in the parents without any previous abnormality of the 
nervous system whatever. The fact, however, that actual 
abnormalities of the nervous system are present in the 
antecedents of 82 per cent, of these cases is proof that 
such does not commonly happen, and the outline which has 
just been given may be taken as a general view of the 
successive steps in the production of idiocy. To give some 
further idea of this, it may be useful to state a few facts 
regarding the brothers and sisters of the patients of whom 
these histories were taken. In this respect the following 
table is instructive. 



Table 8. 

Showing particulars of the Brothers and Sisters of 150 Idiots 

and Imbeciles . 

In the 160 families 

Number of Children Born 

Alive .. .. 1,099 

Dead .. .. 170 




Number now Living 

(A) Healthy .. 

# • • 



.,31 (Delicate .. 

' ' { Mentally affected 

83 | 

245 )' * * 



Number Dead 

Under 1 year.. 

138 ^ 

f« 3 ff • • 


„ 10 .. 


■ .. 



„ 20 „ .. 


Over 20 „ .. 

25 J 

643 466 

Unsatisfactory Satisfactory 
total. total. 


Thus the total number of children born alive in these 
150 families is 1,099, or on an average 7'3 born alive in each. 
The average number in each healthy family in this country 
is 4. The great difference in the number born is therefore 
worthy of note, as is also the large proportion of children 
born dead. Out of this total of 1,099, at the present time 
784 are living, 456 of whom are said to be in good health, 
83 delicate, and 245 mentally affected. A large propor¬ 
tion, therefore, of the brothers and sisters of these 
patients possess such a diminished vitality that they are 
unable to survive the ordinary illnesses of childhood, and 
many of those still living are amongst the most unprofitable 
members of society, possessing well-marked stigmata of 
degeneracy or being idiots or imbeciles. With regard to 
those described as “ healthy,” it must be remembered that 



this is always the parent’s valuation, and therefore the most 
favourable that can be taken; as a matter of fact, my own 
experience is that a large proportion of them are far removed 
from the average standard of mental or physical health, 
being undersized, lacking in the faculty of initiation, and 
often coming under the designation of “ ne’er-do-weels.” 

There is, however, another type of case which at first 
sight appears to be quite distinct from the one just described, 
inasmuch as the patient may be the only one of the family 
showing any sign of deterioration, his brothers and sisters 
being well developed in body and mind. Similar hereditary 
influences exist here also, though not in such marked degree, 
and it is in these cases that they are mostly present on one 
side only. Evidently in these instances the condition cannot 
be attributed entirely to defects in the germinal plasm, as in 
that case other members of the family would also show signs 
of defective development; the question therefore arises as 
to why one alone should be affected. 

It is under these circumstances that I believe the condi¬ 
tion of the mother during gestation to be one of the most 
vital importance to the child ; obviously it is a difficult 
matter to always obtain precise and accurate information on 
this point, but I have been much struck by the fact that it 
is just in these, what one might call sporadic cases of idiocy, 
that nearly all the instances of abnormal condition of the 
mother during pregnancy have occurred. These conditions 
have already been discussed, and it will be sufficient to note 
here that the one most frequently associated with the birth 
of an idiot is a general state of ill-health and exhaustion, 
in the poorer classes often accompanied by a deficiency of 
proper food. In several cases it has happened that during 
this time the father was out of work. 

Apparently under these less pronounced conditions of 
hereditary predisposition, the germinal material, although to 
a certain extent vitiated, is still capable of proceeding to the 
perfect structural development of the embryo, provided no 
untoward circumstances intervene to further embarrass its 
growth, but should there happen at this time any deteriora¬ 
tion in the health of the mother, whereby the blood supplying 



the rapidly growing ovum is considerably modified in its 
nutritive qualities, then incomplete development is very 
likely to happen. As far as my experience goes, the physical 
condition of the mother is of far more importance than the 
mental state, except in the cases in which this may modify 
the physical condition. 

In other instances the same result is attained hy a some¬ 
what different contributing, or as it may be termed, exciting 
factor. One fairly common such is premature birth; if by 
any unfortunate chance this should happen where there 
are already present predisposing factors, even if slight, the 
child is extremely likely to show some mental deterioration 
as compared with his brothers and sisters. In other cases 
prolonged labour, attended with more or less asphyxia, may 
act in the same manner; the temporary obstruction of the 
cerebral circulation need not be enough to give rise to any 
actual lesion, or in a healthy child even to produce any 
damage whatever, but in the present instance it is all that 
is required to interfere with the perfect development of the 
nerve cells, and some degree of weakmindedness is the result. 

In the same way act some of the factors arising after 
birth, such as trauma, convulsions whilst teething, infectious 
fevers, meningitis, &c. It has already been seen that in the 
larger proportion of these cases, ancestral defects are present, 
and the exciting factor probably acts by causing a derange¬ 
ment of the cerebral circulation from which the nerve cells 
are unable to recover. 

It is necessary to bear in mind that factors such as the 
above, are, however, as a rule, only accessory; the real 
origin of the condition lies in the defect of the germinal 
plasm; indeed, in many instances these accessory causes 
may themselves be the outcome of the same defect. 

Group 2 .—Causes Extrinsic to the Germinal Plasm. 


It has been seen that, although in a considerable number 
of cases of amentia there are present injurious factors in the 
surroundings of the patient, yet the actual number directly 



attributable to these is very small. In the large majority 
there is a well-marked predisposition to imperfect develop¬ 
ment, and these accessory factors are to be looked upon as 
accidental complications, perhaps, it is true, occuring more 
frequently than amongst healthy children, since the very 
condition of imperfect development connotes an increased 
liability to secondary morbid processes. 

In a small number of instances in which the hereditary 
predisposition is comparatively slight such factors may act 
in a determining or contributing manner, and in a still 
smaller number, probably altogether not more than 7 or 8 
per cent., they appear to be capable of causing amentia 
unaided; but even in these the arrested mental development 
is usually brought about by tbe frequently recurring and 
severe epileptic fits to which the brain lesion gives rise, and 
they finally end in dementia. 

It has been already mentioned that the brain of a healthy 
child appears capable of withstanding these external injuri¬ 
ous factors to a very great extent; in fact, provided the 
patient be young enough, compensation takes place. The 
evidence in support of such a view is as follows :—Within 
the brain up to 12 years of age there are present in all 
the deeper layers of the cortex a large number of neuro¬ 
blasts, lying between and among the fully developed nerve- 
cells, and even in the brains of normal persons of middle 
age I have repeatedly found numbers of similar cells. It is 
very likely that such neuroblasts represent a potentiality of 
cerebral development which is never realised in the indi¬ 
vidual, and that in the normal brain the provisions of nature 
are far in excess of any call which is made upon them. 
Probably after youth the development of these neuroblasts 
into fully formed nerve-cells cannot take place, it is, how¬ 
ever, upon their presence and the possibility of their being 
gradually brought into play that one bases hopes for the 
future intellectual expansion of the race. Broca, by com¬ 
paring the skulls of 125 persons who lived in the twelfth 
century with those of 125 persons in the same rank of life 
who lived in the nineteenth century, found that the mean 
capacity of the latter had increased by two cubic inches. 


In the healthy individual clinical experience constantly 
shows that lesions of the central nervous system can be 
recovered from, not by the regeneration of the injured 
nervous tissue, for all the evidence goes to prove that such 
does not take place, but apparently by the development and 
bringing into play of other cells to make up for those which 
have been destroyed. That such a compensation can and 
does take place in the motor nerve-cells cannot be denied, 
and this result seems to be achieved by the development of 
the neuroblasts which have just been described, as is strik¬ 
ingly shown by the following instance :— 

In this case a lesion had occurred in the left Rolandic 
area, due (probably) to venous obstruction or haemorrhage 
consequent on difficult birth ; practically all the large motor- 
cells in this area were destroyed, and the fourth cortical 
layer was represented by a very evident, clear, pale zone. 
In the corresponding region of the opposite hemisphere, 
however, these large motor-cells were present to a really 
extraordinary extent, they were all shapes and sizes, and 
more irregularly arranged than normally, but all had well- 
marked Nissl-bodies and dendritic processes. It can hardly 
be doubted that the numerical increase was brought about 
by an attempt to compensate in some measure for the loss 
sustained by the opposite hemisphere. Such a view was 
further supported by the clinical condition of the patient, 
for, in spite of the almost complete annihilation of the large 
motor-cells of the left side, there was very little paralysis, 
the patient could walk quite well, and could do useful work 
with the right hand, the finer movements alone being some¬ 
what defective. In this case the patient’s family history 
was entirely free from any neuropathic taint. There are 
many similar cases of paralysis occurring during early life in 
which almost complete recovery has taken place. 

If compensation of this nature can take place amongst 
the motor cells it is not unjustifiable to think that the same 
may happen in those whose function is higher, provided only 
that the demand be made at a sufficiently early period of life. 
It may be, of course, that in cases of cerebral lesions the 
resulting mental condition is dependent upon the site of the 



lesion, and further pathological research is still desirable in 
this direction; there have been recorded numerous cases of 
porencephaly, cysts, &c., however, in which the patient had 
attained normal mental development, and Schroeder van der 
Kolk mentions a number of instances tending to show that 
a large portion of one hemisphere may be diseased, and yet 
the patient show no mental impairment; clinical experience 
also rather tends to the view that the question of idiocy or 
non-idiocy in these cases cannot be entirely explained by any 
difference in the site of the lesion. 

It is not unreasonable to suppose that in the descendants 
of neuropaths or otherwise degenerate stock the vitality of 
the nerve-cells or neuroblasts is so diminished that they are 
incapable of responding to any extra demand which may be 
made upon them, in fact (as is shown by the microscopical 
examination of cases of primary idiocy) a large number of 
the cells which normally come into action are not sufficiently 
developed for ordinary requirements, and on the whole I am 
inclined to think that in those instances in which a lesion of 
the brain has been produced by one of these external morbid 
factors, the subsequent mental condition is chiefly a question 
of the presence or absence of hereditary influence and of the 
capabilities of the neuroblasts of compensating for the lesion. 

It has been seen then, that not only idiocy and imbecility, 
but also insanity, epilepsy and a large number of neuroses, 
are, in the majority of instances, the result of ancestral 
defects. It obviously follows that any attempt to lessen 
their serious prevalence must be chiefly directed towards the 
morbid states to which they owe their origin. The import¬ 
ance of grappling with Consumption, Alcoholism and 
defective Hygienic Conditions generally cannot be too 
strongly urged, and it is to measures for the amelioration of 
these that we must chiefly look for any appreciable improve¬ 
ment in the mental health of future generations ; at present 
the general public hardly realises to the full the injurious 


effects of these conditions upon the individual and cannot 
be said to have any real conception of their consequences 
upon posterity. 

To refer more particularly to amentia, I have no hesita¬ 
tion in saying that in the large majority of the cases existing 
at the present time we can hope for little improvement of any 
real value. It is true that a certain number of patients of 
the higher grades may be taught various kinds of handicraft 
and in this way they may become partially self-supporting, 
and thus less of a burden to their friends, to the State, and 
also to themselves; but for much beyond this we cannot 
hope, and it cannot be too clearly understood that those 
patients are defective from the very beginning, and that no 
process of education or training will supply such defect and 
enable them to take a place in the world and compete with 
normally developed persons. In the present day it is even 
questionable if such methods of so-called education are not 
carried a little too far, the training of imbeciles is in danger 
of becoming a popular fad, and there is a tendency to allow it 
to run in lines which are altogether unsuited to the require¬ 
ments and capabilities of these patients. 

With regard to the lower grades, it may at once be said 
that the great bulk of them are hopeless, and, to speak quite 
plainly, the great majority of the idiots and imbeciles at 
present existing should have been treated three generations 
back ; it is decidedly questionable whether the many thou¬ 
sands of pounds which are annually spent in this country in 
the training of imbeciles would not be better expended in 
doing more towards the prevention of those injurious con¬ 
ditions above described, which, if unchecked, will assuredly 
give rise to a fresh crop of insanity, epilepsy, and idiocy in 
generations to come. Treatment must be preventive, it 
cannot he curative, and the sooner this is seen in regard to 
amentia the better it will be for the race, although, unfor¬ 
tunately, the doctrine of letting posterity take care of itself 
is one not easily eradicated from the human mind. 

In addition to the above-mentioned diseases there is yet 
one other matter of the deepest importance in the production 
of amentia, and which has hitherto received very scant 



attention: this is the question of marriage. Even apart 
from the subject of nervous degeneration, a large propor¬ 
tion of the disease which at present exists can be traced to 
unsuitable marriages. There are persons of whom it may be 
said almost with certainty that they will transmit disordered 
or enfeebled mental or physical conditions to their children ; 
such should, of course, never marry; others again would 
probably only do so if married to persons of like tendencies. 
On the other hand, an existing taint, if slight, may by suit¬ 
able marriage be much diminished in the next generation, 
and with still further selection may be finally eradicated. 
Although it generally happens that the child bears a greater 
resemblance to one parent than the other, it is nevertheless 
a mixture of both, and this is a natural means by which 
modifications and variations are brought about in the human 
race. The result of any union is, therefore, a step either in 
an upward or a downward direction. 

This being so, the importance of the question of marriage 
cannot be too strongly advocated; it is far too often entered 
upon without any thought beyond the convenience or taste 
of the contracting parties, and, unfortunately, not always 
with even that amount of consideration; but sooner or later 
we shall be compelled to consider its effect upon future 

In some countries legislation towards this end has 
actually been adopted, the marriage of certain persons 
being prohibited, but what may be the practical effect of 
regulations of this kind I have so far been unable to gather; 
probably sufficient length of time has not yet elapsed for a 
clear idea to be gained. It is very unlikely that such a 
method of treatment will ever be legalised in this country 
however, and, even if it were, it is questionable if the results 
would be satisfactory; the relations of people cannot be 
influenced in this compulsory way, and it is more likely that 
beneficial results will be brought about by the education of 
public opinion as to the moral responsibilities attaching to 
the matter. The decrease of crime which has taken place 
during the last fifty years is probably far more due to the 
gradual cultivation of the moral sense, or at all events dread 



of public opinion, than to the deterrent effects of punish¬ 
ment, and I think that it is in the same direction that we 
must hope for most good with regard to the responsibilities 
attaching to marriage. It will, of course, be long before we 
can expect the lower grades of society to be actuated by any 
such motives, but it is undoubtedly the solemn duty and 
privilege of the medical profession and of the Church to 
impress the seriousness of the subject on the general public. 
The Church has peculiar opportunities of rendering incal¬ 
culable service to future generations in this respect by point¬ 
ing out the important issues of the marriage tie, and the 
necessity of being influenced by other than selfish motives. 
The medical profession cannot too strongly warn their 
patients of the evils resulting from unsuitable marriages, 
and should be prepared to give more particular advice on 
this subject, and to decide on the suitability or otherwise 
of any particular case; such a decision must take carefully 
into account the antecedents of each person, and must be 
based upon an accurate knowledge of the factors which are 

It is impossible here to enter more fully into this 
matter, and say what kinds of people should or should not 
be allowed to marry. Unfortunately such advice, even 
when asked for, is by no means invariably taken, but that 
it is occasionally sought is an indication that the public 
are beginning to awaken to a sense of their responsibility 
on the subject. 

Section II. 

The Classification and Varieties of Amentia. 

The classification of the varieties of amentia is by no 
means an easy matter ; various methods have been adopted, 
some based upon the facial or cranial characteristics, others 
upon the presence of pathological lesions; others upon the 
degree of intelligence and capability of response to educa¬ 
tion ; others, again, upon purely psychological grounds, such 
as the amount of attention; and yet others upon a partly 
pathological and partly etiological basis. That proposed by 



Ireland is the one most used in this country ; it is, however, 
open to several objections, since it brings together varieties 
which are really quite different, and separates others which 
should be in the same group ; indeed, it is really little more 
than an enumeration of the various types of idiocy and im¬ 
becility, and can hardly be said to at all show the relation¬ 
ship which exists between the different forms. 

Since many of the pathological conditions are more of 
the nature of accidental complications than the cause of the 
arrested mental development, and since similar pathological 
lesions may in this way complicate quite different varieties 
of amentia, a classification based upon etiology is probably 
more accurate than one based upon pathology. 

Considered, therefore, from the standpoint of causation, 
we have already seen that all cases of amentia may be 
divided into two groups, viz., (1) those due to factors with¬ 
in the germ plasm itself as a result of ancestral defects 
(intrinsic ); (2) those due to factors extraneous to the germ 
plasm ( extrinsic ). To the former group of amentia we may 
give the name Primary or Essential, to the latter Secondary 
or Accidental. It is, perhaps, necessary to say that these 
groups are not synonymous with the terms “ congenital ” 
and “ acquired ” when the latter are used (as they generally 
are) with reference to the existence of the condition before or 
after birth. According to such a division an idiot whose 
condition was due to an injury received during intrauterine 
life, or to some abnormal state of the mother during gesta¬ 
tion ( e.g ., alcoholism), would be described as “congenital,” 
whereas the condition is truly Secondary. On the other 
hand, Primary amentia (due to defects in the germinal 
plasm) may require the contributing action of some factor 
after birth to bring it into prominence (such as trauma or 
infectious fever), and then it would be called “ acquired ” 
under this classification. 

The following brief outline of the chief features of these 
two groups of Primary and Secondary amentia will show 
that not only do they differ in their causation, but also in 
their pathology and symptomatology, and that such a 
division is therefore the most natural basis of classification. 



Primary Amentia. 

In this group the essential condition is one of imperfect 
development, although the actual capabilities of the in¬ 
dividual members may vary within very wide limits ; thus, 
on the one extreme we may have a being whose mental and 
physical states differ but slightly from the normal, to, on the 
other extreme, one who can scarcely be called human at all. 
To this group no less than 90 per cent, of all idiots and 
imbeciles belong. The mental condition in the worst cases 
is but part of the general failure of development of the 
whole organism, as is fully shown by the existence of the 
numerous physical defects and abnormalities which we call 
“ stigmata of degeneracy.” In the milder cases the higher 
mental functions alone may suffer. 

The pathological condition will be more fully referred to 
under the next section ; generally it is as follows: the brain 
may vary greatly in size and external appearances* but on 
the whole is smaller and more simply convoluted than 
normally ; in the mildest cases our present means of micro¬ 
scopical examination may reveal little change, but in the 
more pronounced types the central nervous system is 
characterised by a paucity of cells which are badly-arranged 
and ill-developed, and by a diminution in the number of 
fibres composing the cerebral association systems. The hori¬ 
zontally coursing bundles of fibres known as the tangential 
layer, and the super- and inter-radial bundles are strikingly 
diminished when compared with the healthy brain. Super- 
added to this imperfect growth there are frequently other 
gross abnormalities and more or less severe morbid processes 
(such as porencephalus, hydrocephalus, etc.), which may 
tend to bring about a degeneration of the already imperfectly 
developed nerve-structures, and so to produce dementia. 

Amongst the cases of primary amentia there are five dis¬ 
tinct varieties which may be distinguished by the presence 
of certain characteristics. The first is a simple arrested 
development, and this variety may therefore be called 
“ simple ” idiocy or imbecility. In the second and third 
(microcephalies and mrongolians) the arrest has taken a more 



particular form, and produced distinct types, the skull as a 
rule being smaller than normal. In the fourth and fifth 
(hydrocephalics and sclerotics) it is further complicated by 
the addition of pronounced pathological changes, and in these 
the skull is usually larger than normal. It must, however, 
be remarked that secondary morbid processes may accompany 
any of these varieties, hut only in the two latter are they 
present to such an extent as to justify one in using them as 
a means of sub-classification. The following, therefore, are 
the Varieties of Primary Amentia :— 

(1) Simple. (2) Microcephalic. (3) Mongolian. (4) Hydrocephalic. 

(5) Sclerotic. 

Secondary Amentia. 

In the cases comprising this group, the arrested mental 
development is purely accidental and symptomatic of some 
cerebral or other morbid process ; such process may be the 
result of trauma, asphyxia neonatorum, sunstroke or some 
toxic condition, or of a disturbance of the thyroid gland, or 
of an imperfection of the organs of special sense. When a 
lesion of the brain is present, it not only arrests any further 
intellectual growth, but by its continued presence frequently 
also induces a degeneration in those neurones already par¬ 
tially developed, and so produces dementia. The cases in 
this group comprise at the most about 10 per cent, of all 
instances of idiocy and imbecility. 

It has been seen that in a considerable number of these 
cases, the actual arrest is due to the frequent recurrence of 
epileptiform convulsions, and it must again be definitely 
stated that it is rare for one of these external causes 
(unaided by hereditary morbid influences) to give rise to 
amentia, except through the medium of epileptiform con¬ 

The pathological conditions underlying this group are 
various, and many of them yet imperfectly ascertained. 
The cases likewise differ greatly in their clinical appear¬ 
ances, chiefly with regard to the rapidity with which 
dementia supervenes. The group contains the following 
eight varieties, which may be divided into two classes:— 



Varieties of Secondary Amentia. 

Amentia due to 


r (1) Epilepsy. 

(2) Encephalitis. 

(3) Hydrocephalus. 

(4) Trauma. 

(5) Infantile Cerebral Degeneration. 
. (6) Juvenile General Paralysis. 

\ (B) 1 W A-thyroidism (Cretinism). 
' ’ ( (8) Sense deprivation. 

In Class (A) the process present is really more one of 
degeneration and dementia, and the arrest of development 
which necessarily takes place in the course of this is purely 
an incidental circumstance ; as far as prognosis is concerned 
these cases are amongst the worst. In Class ( B ), there is, 
as a rule, no dementia, the condition being simply one of 
arrested intellectual development, and entirely dependent 
upon external causes. Want of space prevents any further 
description of these clinical varieties. 

In the following Table of Classification I have attempted 
to arrange all the varieties of amentia on this plan; it is 
not suggested that such a scheme is anything like perfect, 
but it is claimed that it gives a clearer conception than 
is otherwise obtainable of the relations existing between 
the etiological factors, the pathological conditions and the 
clinical aspects in the many varieties of this disease. 

In the first column a division is made into these two 
main groups, primary and secondary. In the next column 
are given the various etiological factors, arranged in three 
classes; in Class (A) they are hereditary influences only, and 
the amentia to which they give rise is purely primary; in 
Class ( B ) the factors are epilepsy, toxic, trauma and sunstroke ; 
in the majority of instances these are simply contributory 
to those in Class (A), and the amentia is therefore primary; 
occasionally however, they may be the sole cause of the 
arrested mental development, which is then secondary. It 
will, therefore, be seen that the two groups overlap in this 
class. In Class ( C), the factors are entirely extraneous, and 
are the sole cause of the amentia, which is therefore purely 



In the next column are given the various pathological 
conditions present in these different classes; and in the last 
column is given a short general clinical description of the 
class, with an enumeration of the varieties of amentia which 
occur in it. 

Practically the only difficulty which arises is in Class ( B ), 
in which the overlapping takes place, and here it is impor¬ 
tant to remember that whilst these factors may occasion¬ 
ally produce amentia unaided, they more commonly act as 
contributory influences to those in Class (A), having been 
necessary to bring about a failure of compensation, or at 
times being simply accidental complications. It will be 
seen that in these three classes, the importance of here¬ 
ditary influences becomes less marked from above down¬ 
wards, being the sole cause in (A), the chief factor in (B), 
and absent in ( G ). 

Having allotted the case to its proper group, class and 
variety, it is then perfectly easy to specify the degree of 
mental ability by describing it as high, medium, or low 
grade. This is, indeed, absolutely essential for purposes of 
education and administration, but the attempt to arrange 
cases of amentia with regard to their intellectual capabilities 
only, without any reference to their place in the natural 
order of amentia, is entirely unscientific and misleading. 

With regard to epileptic idiocy, this term should, strictly 
speaking, be confined to those cases in Class ( B ) in which the 
epilepsy is the cause of the condition; it is, however, very 
commonly applied to any and every case of amentia asso¬ 
ciated with epilepsy; this is apt to lead to much confusion, 
especially when we consider that about 50 per cent, of 
all idiots and imbeciles are subject to epileptic attacks of 
varying frequency and severity, and that nearly all the 
varieties may be so affected. I have already referred to the 
great prevalence of epilepsy in nearly all the varieties of 
secondary amentia; its incidence in the primary group is 
evident from the following particulars, which Dr. Beresford 
was good enough to collect for me, of the patients admitted 
to Darenth Asylum during the years 1898,1899, and 1900:— 



due to causes 


the germinal j 
plasm. I 



accidental l 

due to causes j 
extrinsic to the i 
germinal plasm. 

is degrees of amentia , ranging between gross idiocy , imbecility , and 
j slighter forms of mental weakness. 

ata of degeneracy are present , and, as a rule, education leads to more 
iss improvement in their mental condition . 
gross forms the patient is unable to speak, to wash, or even feed 
self, and has no idea of personal cleanliness ; in the mildest forms 
condition is more one of mental instability, little change can be 
irved in the structure of the nerve-cells, but they seem incapable 
unctioning satisfactorily. Such high grade imbeciles are capable 
arning their own living, but are liable to acute outbreaks of 
nity, to which their first appearance in the asylum is frequently 

Brtain proportion the condition is complicated by epilepsy or some 
1 of paralysis 

llowing varieties occur :— 

1. Simple Idiocy. 

2. Microcephalic (also Scaphocephalic). 

3. Mongolian. 

I. Hydrocephalic. 

5. Sclerotic (“ Hypertrophy of the brain ”). 

! is degrees of arrested mental development , as a rule not so pro- 
I iced as in Class (.4), and subsequently followed by progressive 
I notation and dementia. Education leads to little or no improvement. 
i 5 majority paralysis and epilepsy are present; the latter is fre- 
I ltly at first Jacksonian in character, but afterwards becomes 
| ral. 


|]lowing varieties occur : — 

, 3. Epilepsy. 

Amentia due to 

2. Encephalitis. 

3. Hydrocephalus. 

4. Trauma. 

5. Infantile Cerebral Degeneration. 

6. Juvenile General Paralysis. 

t it must be remembered that in a juvenile general paralytic some 
tia may have existed from birth, owing to causes in Class (4), the 
leration is super-added to this. 

1 ndness, Deaf-mutism. &c., with Amentia (usually mild). Educa- 
| results in great improvement. 

j pansion and development of the mind cannot take place owing to 
I sensory pathways being closed, in this way communication with 
outside world (the chief means by which the human mind is 
loped) is cut off. Amentia actually due to such a condition is very 
; but it is not unusual to find a primary idiot suffer from some 
j ory defect, both conditions being the result of the same imperfect 
i development. 

etinism. Thyroid treatment jnvduces great improvement. 

To face p. 380. 



Variety of Amentia. 





(1) Simple . 



(2) Microcephalic 



(3) Mongolian. 



(4) Hydrocephalic . 





Total .. .. 227 

The extreme rarity of fits in the mongolians is very 
singular and worthy of note; indeed, I have only seen two 
such patients who were the subjects of epilepsy. 

Paralysis may also accompany several distinct varieties 
of amentia, and since it cannot be urged that this is ever the 
cause of the arrested mental development, being itself but a 
symptom, there is less justification for the term “ paralytic 
idiocy ” than for that of “epileptic idiocy” ; it would be more 
logical to speak of such a variety of amentia with or without 

Such a term as “ rachitic idiocy ” should be abolished, 
since there is no reason for thinking that rickets is ever the 
cause of amentia. 

There is one other condition which is such a frequent 
and important accompaniment of the higher grades of prim¬ 
ary amentia that it must be briefly referred to: this is 
insanity. Such a complication is rarely seen in the special 
idiot institutions ; it is, however, very common in the general 
asylums, and out of 200 cases of imbeciles whom I examined 
in these latter institutions, more than half either were or 
had been insane. The insanity may be of the emotional or 
ideational type, and in many cases hallucinations and de¬ 
lusions are present; recurrences are frequent and final 
dementia is common. Since I have elsewhere described 
these cases more fully (vide ref.), it is unnecessary to say 
more in this place. 



Section III. 

Pathology.—Notes on the Microscopical Examin¬ 
ation of Twelve Cases of Amentia. 

Opportunities for the microscopical examination of suit¬ 
able cases of amentia are by no means frequent, largely 
owing to the extreme solicitude with which these patients 
are now cared for in the various institutions set apart for 
their reception. I have, however, been able to make such 
an examination in twelve cases, and it seems worth while 
recording the results in this paper, more particularly as the 
cases embrace several varieties of the affection, and the 
conditions present have considerable bearing upon some 
points which have been alluded to in the etiological and 
clinical portions of this article. 

At the outset it may be stated that the microscopical 
appearances fully coincide with the division into primary and 
secondary amentia which has been made, cases of primary 
amentia being characterised by evidence of imperfect or in¬ 
complete development, and those of secondary amentia by 
degenerative changes. In cases of primary amentia to which 
dementia becomes superadded (such as from general paralysis, 
epilepsy, &c.) these two conditions of imperfect development 
and degeneration co-exist; and in such it is by no means an 
easy matter to distinguish the imperfectly developed cell, as 
the degeneration present tends to mask that condition ; a 
similar difficulty is experienced in making a clinical diagnosis 
in such cases, the original idiocy or imbecility often being 
only ascertainable after a careful enquiry into the attain¬ 
ments of the patient prior to the onset of the dementia; 
or, occasionally, by the presence of pronounced stigmata of 

In the following pages an account will be given of the 
microscopical features of the nerve-cells, nerve-fibres, neuro¬ 
glia and vessels of these twelve cases, with some general 
remarks respecting the pathology of amentia. This will be 
followed by a brief abstract of each case, and a summary 
showing the important points in tabular form. 



Primary Amentia. 

The skull .—In most of the cases of primary amentia ex¬ 
amined this is thicker and denser than normal, the diploe 
being practically non-existent. This condition of the skull 
was formerly considered to be the cause of the imperfect 
mental development, and the view that microcephalic idiocy 
is brought about by premature synostosis of the cranium is 
not even yet obsolete. This, however, is clearly to put the 
cart before the horse, and such a view cannot logically be 
maintained. It may be stated that numerous cases of micro¬ 
cephaly have now been recorded in which the sutures were 
not closed, and in the instances in which they are it is pro¬ 
bably due to the very fact that the brain has ceased to grow. 
That the increased thickness of the skull is simply compen¬ 
satory for the small size of the brain is also shown by the 
fact that it is chiefly the inner table which is involved, and 
that if one hemisphere be less developed than the other, the 
corresponding half of the skull (chiefly the inner table) 
becomes proportionately increased in thickness. Further, 
in some cases of hydrocephalus, or enlargement of the brain 
due to other causes, the skull increases in size and becomes 
very much thinner, at times, indeed, being insufficient to 
cover the encephalon but for the formation of Wormian 
bones. One cannot help thinking, therefore, that the 
general shape and dimensions of the skull are chiefly in¬ 
fluenced by, and closely follow, those of the contained 
cerebral matter. 

The membranes .—In the cases in which dementia has 
supervened upon the amentia the membranes are found to 
be more or less thickened, the dura mater sometimes being 
firmly attached to the vertex of the skull and the pia-arachnoid 
being opaque and stripping with unusual readiness from the 
surface of the brain, in the widened sulci of which exists 
considerable excess of cerebro-spinal fluid. These con¬ 
ditions, however, are those of dementia and not of amentia, 
in the ordinary cases of which, where no pathological con¬ 
dition or gross abnormality of development is present (such 
as porencephaly, cysts, &c.), the membranes are normal. 



Brain .—In the milder types of imbecility the naked eye 
examination of the brain frequently reveals but little depar¬ 
ture from the normal; the convolutions may be less complex 
than usual, but in other respects there is nothing to attract 
attention, and the size and weight may be quite equal to the 

On the other hand, in the pronounced forms of idiocy 
the naked eye examination of the brain usually affords 
ample evidence of that condition, the organ being small, 
imperfectly and irregularly convoluted, with occasionally a 
greatly altered consistence. The hemispheres may be un¬ 
equal in size, sometimes markedly so, and various forms of 
local agencies and other abnormalities may he present; in 
other cases definite morbid lesions also exist, such as hydro¬ 
cephalus, localised softening, &c. 

It is unnecessary in this place to deal more particularly 
with the many abnormalities which may be met with in the 
idiot’s brain, beyond remarking that they may all be referred 
to one of two groups, viz. (1) those due to errors of de¬ 
velopment, (2) those due to secondary morbid processes. 
The former are but a further and more gross expression of 
the incomplete development, which will presently be de¬ 
scribed as existing in the nerve-cells; the latter conditions 
appear especially prone to affect the imperfectly developed 
brain. In my opinion, it is very rarely that any of these 
conditions can be considered as the cause of the mental 
deficiency (although—generally by giving rise to epilepsy— 
they may in a few instances produce dementia with some 
incidental arrest of mental development), since a difference 
of several hundred grams may exist between the two hemi¬ 
spheres of the brain, owing to porencephaly, cysts, &c., with 
very little or even no appreciable mental impairment. It is, 
of course, possible that in a small number of cases mental 
deficiency may be brought about by one of these lesions 
occurring in early life, and depriving the brain of a large 
number of cells, if at the same time the developmental 
capacity of the remaining cells is so limited (by inherent 
defects of the germinal plasm) that compensation cannot 
take place in the manner described under “ Etiology.” 



This, however, is due to the condition of the nerve-cells, and 
therefore, strictly speaking, these morbid conditions do not, 
as a rule, belong to the pathology of amentia, but are more 
of the nature of complications. Incidentally it may be 
noticed that in cases of focal lesions of the brain occurring 
at an early age there is an arrest in the development of 
those portions of the nervous system whose function is 
correlated to the diseased part. 

Nerve-cells .—In all the cases examined there are import¬ 
ant alterations in the condition of the nerve-cells, and the 
amount of change discoverable under the microscope bears a 
distinct relation to the degree of mental deficiency noticed 
in the patient during life. The abnormalities of the nerve- 
cells are the following:—(1) Numerical deficiency ; (2) irre¬ 
gularity in arrangement; (3) imperfect development of 
individual cells. 

(1) Numerical deficiency .—Although an actual enumera¬ 
tion of the nerve-cells present in these cases cannot be 
made, I am convinced, from the careful examination of a 
large number of sections, that the cells composing the gray 
matter of the cerebral cortex are decidedly fewer than in the 
normal brain. In some cases, indeed, this paucity of cells is 
so marked that it brings about a decrease in the thickness of 
the cortical gray matter which is obvious to the naked eye. 
Further, although the cells of all the layers appear to be 
fewer than normal, it appears to be the small and medium¬ 
sized pyramidal cells which are most diminished in number. 

(2) Irregularity in arrangement .—Notwithstanding the 
statement of Hammarberg, I certainly think that irregularity 
in the arrangement of the nerve-cells of the cerebral cortex 
is far more commonly met with in the brains of the mentally 
defective than in those of normal intelligence. The con¬ 
dition was present in all the cases examined, the pyramidal 
cells being apparently most affected in this way, although 
this, of course, may simply be due to the fact that the form 
of these cells is such that any irregularity would be more 
readily noticed. In the pyramidal layer of all parts of the brain 
are to be seen numbers of cells lying obliquely, horizontally, 
or completely upside down, and whose apical processes point 




in all directions; these are seen in sections stained by the Sil¬ 
ver method, as well as in Nissl and Polychrome specimens. 

(3) Imperfect development of the nerve-cells .—With the 
object of comparing the appearance of the nerve-cells in 
amentia with those occurring in a healthy brain at various 
periods of its development, a microscopical examination 
was made of different portions of the cerebral cortex from 
embryos of seven and eight months, and from children of 
two and four weeks old, which were kindly placed at my 
disposal by Dr. Bolton. In these brains the various stages 
in the development of the nerve-cell can readily be traced, 
and are as follows : in the embryo of seven months lamina¬ 
tion has not yet appeared, and the cells of the frontal lobe 
are represented by large numbers of neuroblasts ; these are 
small round cells, possessing a close, readily-stained intra¬ 
cellular network, and quite devoid of processes; they are 
imbedded in a ground substance which, in the hardened and 
stained section, somewhat resembles the grain in marble 
(Plate I., fig. 1). In the eight months embryo the neuro¬ 
blasts are somewhat larger, and the intracellular network is 
less close, so that the cell does not stain quite so dark, but 
otherwise it does not differ from that just described, and 
although the coloured ground substance looks somewhat like 
protoplasmic processes belonging to the cell, a close examina¬ 
tion shows that the neuroblast is really devoid of processes 
(see Plate I., fig. 2). At this age lamination is just becoming 
evident. By two weeks after birth the cell has advanced very 
considerably in its development, and may now be readily 
recognised as a nerve-cell; it possesses a body, although the 
protoplasm composing this differs greatly from that of the 
mature cell, being very vacuolated, and liable to break away 
from the nucleus; as a rule an apical process is present in 
the cells of the pyramidal layer, and occasionally other 
processes exist, but the apical one is always the best devel¬ 
oped, and appears to be the earliest formed (see Plate I., 
fig. 3). 

The above description applies to the cells in the frontal 
lobes of the brain only; in other regions, the motor in 
particular, development is somewhat more advanced, and in 


the eight months embryo medium-sized pyramidal cells, and 
also Betz cells can readily be recognised, although possessing 
very few processes, and being devoid of Nissl-bodies. 

Referring now to the condition in primary amentia, in 
several of the cases examined there exist a large number of 
cells which have the following characteristics: the nucleus 
is large and globular or ovoid in shape; the intranuclear 
network is distinct, and in addition there are often two or 
more fine lines which divide the nucleus into three or four 
compartments ; the nucleolus is eccentric, so that in some 
sections it cannot be seen; the cell body is represented by a 
few irregular strands of protoplasm, generally without any 
definite cell wall, and often without processes, or occasion¬ 
ally with a slight attempt at an apical one. Such cells rep¬ 
resent the most imperfect form to be met with, and in the 
degree of their development correspond very closely with the 
neuroblasts which have just been described as present in 
the brain shortly after birth. In addition to these cells there 
are others whose development is slightly more advanced, 
and which possess a distinct cell body and recognisable pro¬ 
cesses, although the latter are not nearly so numerous as 
in the normal cell and their branches are exceedingly few, 
the apical process being invariably better developed than 
the others. In all of these the nucleus is large, ovoid, or 
pyriform, and the nucleolus is eccentric (see Plate I., figs. 4, 
5, and 6, and Plate II., figs. 1, 3, and 4). 

I think it cannot be doubted that the above appearances 
represent a condition of imperfect development; the cells 
retain many of the characters which are normally present 
at an earlier period of life, and they correspond very closely 
with those existing in localised areas of agenesis such as 
sometimes occur in the idiot’s brain, as in Case No. 2. Such 
imperfectly developed cells were found in all the cases of 
primary amentia examined, in some of them being present in 
all parts of the cerebral cortex, although generally to greater 
extent in the frontal and parietal regions than elsewhere, and 
in far greater number in the layer of small pyramids than in 
any other layer. Their appearance agrees very closely with 
the descriptions of other writers, especially that of Bevan 



Lewis, who, as early as 1879, drew attention to the presence 
of similar cells in the second and third cortical layers; he 
states, however, that these embryonic cells were only found 
in cases of amentia which were accompanied by congenital 
epilepsy, and not in cases of pure idiocy or imbecility with¬ 
out epilepsy. This is probably due to the fact that methods 
of staining at that time were not quite so advanced as in the 
present day, since these cells were unquestionably present in 
my cases of amentia without epilepsy. 

The above appearances are seen in Polychrome and Niasl 
stained sections; in addition, I examined the cortex of 
several cases by means of Bolton’s modification of the Silver 
method, and in these sections not only was great irregu¬ 
larity in the arrangement of the cells observed, but also the 
processes and their branches and gemmules were decidedly 
fewer than normally. It seems necessary to mention this 
fact, although personally I am not inclined to attach much 
importance to it, as I doubt whether the silver method is 
sufficiently reliable for such comparative examinations. 

There is another condition of the nerve-cell which is 
exceedingly common in these cases, namely, the presence of 
pigment. In the lowest developed cells above described 
such does not occur, but in a large number of those which 
are somewhat more advanced and which possess a well- 
marked cell body, there occurs a considerable deposit of 
granular pigment; generally this is situated at one angle of 
the cell, away from the nucleus, but at times it is so abun¬ 
dant as to almost completely fill the cell; the pigment 
is yellow in colour in Nissl or Polychrome sections, but 
appears dark-brown or almost black in those stained with 
Marchi’s fluid, and hence gives to these sections a most 
striking appearance. In several of the cases it is particularly 
pronounced in the cells of the Hippocampus (see Plate III., 
figs. 1 and 2). The exact nature and significance of this pig¬ 
ment is unknown, though the reaction with Marchi’s fluid 
would suggest that it was of a fatty nature; a similar condi¬ 
tion, but to nothing like the same extent, is frequently found 
in the central nervous systems of patients who have suffered 
from chronic nervous disease ( e.g ., disseminated sclerosis, 


amyotrophic lateral sclerosis, progressive muscular atrophy, 
chronic insanity, &c.). Its occurrence in these conditions as 
well as in the imperfectly developed cells of amentia would 
appear to warrant a belief that it is an indication of defec¬ 
tive function, the metabolism of the cell being insufficient 
to get rid of all the waste products, which, therefore, accu¬ 
mulate in the form of this black pigment. Its presence is 
nearly always associated with a diminution in the size and 
number of the Nissl-bodies. 

Fibres. —The method adopted for staining the fibres has 
been as follows: after thoroughly impregnating the tissue 
with Marchi’s fluid it was cut in celloidin, and the separate 
sections then mordanted for forty-eight hours in a solution 
of iron alum ; they were then stained with Kulschitzky’s 
fluid, and afterwards slowly differentiated with Pal’s solution. 
The possibility of bleaching out some of the finer fibres by 
this method is not unknown to me, but if carefully per¬ 
formed I believe it to be still the most satisfactory method 
for work of this nature, and one can be more sure-of obtain¬ 
ing sections of uniform thickness by cutting in celloidin 
than by freezing, an important point where comparisons 
have to be made. Stained as above, the sections show a very 
definite diminution in the number of fibres of the horizontal 
systems of the cortex; generally speaking, the most marked 
alteration occurs in those composing the outer line of Bail- 
larger, next in the super- and inter-radial groups, and to 
somewhat less extent in the superficial tangential fibres 
(see fig. 1). The frontal and parietal regions are more 
affected than other portions of the brain, although it is to 
be remarked that for some reason or other the fibres in these 
two regions normally do not stain so readily as elsewhere; 
making due allowance for this fact, however, I think there 
is no doubt that the frontal and parietal regions are far 
poorer in fibres than they should be. In the motor region 
the change is comparatively slight, and in the occipital 
region there is practically no diminution. 

Neuroglia .—The condition of the neuroglia varies very 
considerably in these cases; in some of them there is no 
increase whatever, in others a slight proliferation is present, 



and in a few there is such an enormous overgrowth that it 
has justified the formation of a distinct variety of amentia 
(sclerotic) (see Plate II., fig. 2). In these latter cases the 
excess of neuroglia may be in the form of a diffuse irregular 
overgrowth, a definite band on the surface of the brain, or 
circumscribed nodules. 

I have now examined three cases of sclerotic amentia, 
and in all of these quantities of neuroblasts are present, as 
well as many nerve-cells in a typical condition of incomplete 
development (See Plate II., figs. 1 and 3), so that it seems 
justifiable to regard the neuroglial overgrowth as to a certain 
extent a secondary condition, due to the imperfect develop¬ 
ment of the higher elements; not that it is exactly a sub¬ 
stitution product, but rather that its activities of growth 
are less cheeked in proportion as the development of the 
nerve-cells is arrested. Other influences, however, than 
mere arrested development of the nerve-cells would seem 
to play a part in the production of sclerosis, since in many 
cases of amentia there is no neuroglial increase whatever, 
and it may be remarked that in cases of degeneration, such 
as general paralysis, similar variations exist with regard 
to the amount of neuroglia present. Once the process has 
been initiated, there seems in some instances a tendency to 
indefinite progression, just as occasionally happens in the 
secondary sclerosis following diseases of the nervous system, 
a fact first pointed out by Charcot. 

In some of the sclerotic areas of one of these cases the 
remains of old haemorrhages were found, and such might 
possibly be considered as the cause of the growth. This can 
hardly be so, however, since there w r as no sign of any such 
condition in any of the other areas, the haemorrhage, there¬ 
fore, is probably subsequent to the overgrowth. 

Vessels .—The most noticeable feature about the vessels is 
the presence of deposits of black pigment wfithin the endo¬ 
thelial cells of the capillaries; this is arranged around the 
nuclei of the cells, has the form of irregular granules of vary¬ 
ing size, and appears to be identical with that in the nerve- 
cells (see Plate III., figs. 3 and 4). On casual examination 
this pigment might be mistaken for fatty products of de- 


generation collected within the perivascular lymphatics, but 
more careful examination shows that the granules are really 
deposited within the endothelial cells; also recent degenera¬ 
tive changes do not exist in either the nerve-cells or fibres. 
The condition has an even greater resemblance to what is 
usually described as fatty degeneration of the capillaries, but 
there is no doubt that in these cases it is really pigment. It 
is not found in the vessels unless the nerve-cells are similarly 
affected, although this latter may happen without any change 
in the vessels. In some of the smaller arteries a similar con¬ 
dition is present in the cells of the adventitia. 

Beyond the few small hiemorrhages present in the areas 
of sclerosis already described there are no vascular changes 
of a structural nature. 

Secondary Amentia. 

Two cases of this have been examined, in both of them 
the mental condition being the result of epilepsy occurring 
in early life, which is certainly the most common cause of 
secondary amentia. 

In these two cases more or less dementia was also 
present, and as a description will be found in the appended 
abstract it is unnecessary to say much regarding them in 
this place. The fact may be emphasised, however, that 
the microscopical changes are those of degeneration (see 
Plate II., figs. 5 and 6), and are quite different to those 
occurring in primary amentia, although in one of the 
cases there are in addition slight indications of imperfect 
development of the nerve-cells. The degeneration is of a 
chronic nature, there being no evidence of acute change, 
and no recent degeneration observable in Marchi-stained 
sections. The cells chiefly affected are the small and 
medium-sized pyramids, and a considerable deposit of 
black pigment, like that occurring in the cells in primary 
amentia, is also present. The same groups of horizontal 
fibres also show a numerical diminution (see fig. 1). 

The description here given of the condition of the 
nerve-cells in primary amentia is largely confirmatory of 



previous observations, and some of the facets are by no 
means new, and the evidence now appears to be sufficiently 
conclusive to enable one to say that this form of mental 
deficiency is due to a numerical diminution, an irregular 
arrangement, and an imperfect development of the nerve- 
cells of the cerebral cortex. It must be remarked, however, 
that neuroblasts are present in the normal adult brain, also 
that cells which appear to be of perfect development may be 
seen in the brain of the idiot, even of the most pronounced 
type ; but whereas in the former the number of neuroblasts 
is comparatively small and the great majority of tbe cells have 
attained complete development, in the latter the reverse is 
the case, the bulk of the cells being in an immature con¬ 
dition, and many of them also showing further indications 
of defective function in the presence of considerable deposits 
of pigment. Further, the proportion of such immature 
cells appears to be directly related to the degree of mental 
deficiency, and in the milder forms of imbecility the micro¬ 
scopical condition is rather one of paucity of cells and of 
irregular arrangement than of pronounced imperfection in 
the individual cells. 

Bevan Lewis stated that the embryonic cells which he 
described were particularly evident in the second and third 
cortical layers (the small and medium sized pyramidal cells), 
and my own observations are entirely in accordance with 
this. Incompletely developed cells occur, it is true, in all 
the cortical layers, but the small and middle pyramidal cells 
show far greater evidence of this than do the cells in other 
layers. Considering, moreover, the fact that it is these cells 
which are normally amongst the latest to attain their full 
development, and also that as a result of my own observations 
upon several cases I find they are the earliest and most 
affected in forms of dementia resulting from epilepsy, chronic 
insanity, &c., there seems strong reason for concluding that 
it is these cells which subserve the highest mental functions. 
In general paralysis other cell layers are also involved, 
especially the cells and fibres of the efferent path, but this 
disease is not an example of pure dementia. It is not im¬ 
probable that the anatomical basis of idiopathic epilepsy , 



and possibly also of insanity, will ultimately be proved to 
consist in an inherited instability, defective metabolism, or 
tendency to premature degeneration of these cells, the actual 
exciting cause of the outbreak being supplied by almost any 
slight disturbance of the bodily health. The convulsions 
are explicable by the diminished inhibition thus brought 
about, the various psychoses by their disordered action, and 
dementia by their death. 

VVith regard to the fibres of the cortex less work has 
been done, the most important probably being that of Kaes; 
he drew attention to the fact that the horizontal fibres 
gradually increase in number up to the fortieth year, and 
that afterwards a diminution takes place. It is therefore 
of interest to note their deficiency in these cases of amentia, 
and also, it may be remarked, in cases of dementia; in these 
conditions, with the exception of general paralysis, the 
superficial tangential fibres appear to be less affected than 
the other groups, and it is probable therefore that their 
function is of a somewhat lower order than the fibres 
composing the super-radial group and the outer line of 

Incomplete development appears to be chiefly confined 
to the cortex of the brain, and in all but the most pronounced 
cases the cells of the basal ganglia, cerebellum, and spinal 
cord are fairly normal. It appears to be highly probable 
that the cortical regions most affected are those of the frontal 
and parietal lobes, although further observations in this 
direction are greatly to be desired. 

On the other hand, in the majority of cases of secondary 
amentia the anatomical condition is one of degeneration 
occurring at an age when the mental faculties are not yet 
fully developed, and thus incidentally producing arrest. 
This degeneration, if not actually restricted to, is much more 
pronounced in, the same cell layers and regions of the brain 
as are the site of the imperfect development in primary 
amentia. It is either of a slowly progressive nature, as in 
the cases due to epilepsy, encephalitis, hydrocephalus and 
trauma, or it may run a much more acute and rapid course, 
as in infantile cerebral degeneration and juvenile general 



The pathology of secondary amentia is really therefore 
a two-fold question, embracing, firstly, the causes which pro¬ 
duce the local lesions of the brain, and secondly, the manner 
in which these act in bringing about amentia. With regard 
to the local lesion, the probability is that this is either due 
to vascular change, such as embolus, haemorrhage, or 
thrombus, or to some toxic body, like that in meningitis, 
scarlet fever, acute anterior polio-myelitis, &c., though 
some of these poisons may act by bringing about vascular 

Much less is known as to the way in which these local 
lesions give rise to amentia, but since in the majority of 
cases epilepsy or epileptiform convulsions result, it is 
possible that degenerative changes have been produced in 
those cell layers concerned with inhibition and the higher 
mental functions. The convulsions in the first instance 
may be Jacksonian in nature, and not attended by loss of 
consciousness, but subsequently they become indistinguish¬ 
able from true epilepsy, finally ending in more or less 

In some instances the degenerative process may be due 
to hereditary influences, as in idopathic epilepsy; or to an 
intoxication during intra-uterine life, such as that of syphilis, 
producing general paralysis. 

It need scarcely be observed that the two best examples 
of secondary amentia, viz., those due to athyroidism and to 
sense deprivation, are not of this degenerative nature, the 
condition here being probably simply and purely that of 
arrested development. 

Abstract of Cases. 

Case 1.—(A. D. P., female, No. in series 199.) Primary 
amentia; simple variety; low grade (idiot); with occa¬ 
sional epileptic fits; no dementia. 

Family history. —Not recorded, no friends living. 

Clinical. —Idiotic from birth and subject to chorea, but not 
epileptic. Admitted to asylum aged 10; very little intelli¬ 
gence; unable to speak or wash or dress herself, and with no 
idea of personal cleanliness. She did not improve in any way, 


and remained practically unchanged during the whole of her 
life. She showed scarcely any curiosity or power of attention 
or imitation; she never learnt to speak, but was in the habit 
of constantly making a peculiar noise like the braying of a 
donkey; she was never able to wash, or dress, or feed herself 
without assistance, and was always of filthy habits. She was 
always a source of great trouble to the nurses and all who 
came into contact with her, needing almost constant attention, 
and at times she became most excited, violent and aggressive. 
Very occasionally (about every three months) she had two or 
three epileptic fits. The patient died at the age of 36 of 
gangrene of the lung, the result of aspiration of a small por¬ 
tion of food. There were numerous stigmata of degeneracy. 
Circumference of skull, 20 inches. 

Post-mortem appearances .—The skull was very thick and 
dense, there being no diploe. The dura mater was normal; the 
pia-arachnoid was slightly opaque along the lines of the larger 
fissures, but was not thickened, and stripped naturally. The 
brain was small, weighing (with the pons and cerebellum) 1,022 
grammes; the two hemispheres were symmetrical but decidedly 
simply convoluted. There was no wasting and no further change 
obvious to the naked eye. The vessels and sinuses were healthy. 
The kidneys were deeply fissured owing to a partial persistence 
of their original lobulated condition; there was also a prolapse 
of the rectum. 

Microscopical examination. —Sections of the brain were 
examined from the following regions: the middle and lower por¬ 
tions of the first frontal, the top of the ascending frontal (leg 
area), Broca's, supramarginal, and temporo-sphenoidal convolu¬ 
tions, the hippocampus, and the tip of the occipital lobe; also 
from the basal ganglia, cerebellum, medulla and spinal cord. 

In all parts of the brain cortex alterations are present, but 
more marked in some regions than in others; on the whole, the 
least departure from the normal occurs in the occipital and 
temporo-sphenoidal lobes, and the greatest in the frontal region. 
As a rule the different cortical layers can be readily distinguished, 
but in places this is somewhat difficult under a low power owing 
to the incomplete differentiation of the cells composing them. 
In sections stained by the Nissl and polychrome methods the 
principal condition seen is an incomplete development of the 
nerve cells, especially those of the second and third cortical 
layers (small and medium sized pyramids). These cells are 
smaller and fewer than normal, and are irregularly and imper¬ 
fectly shaped; as a rule the nucleus is large, the chief deficiency 



being evident in the cell body, many of them indeed being 
little better than neuroblasts. In the deeper cortical layers 
there are also many cells in a condition of imperfect development, 
and there is also much irregularity in their arrangement; they 
lie in all directions—sideways, obliquely, or completely upside 
down; there can be no doubt on careful examination, however, 
that the greatest amount of imperfect development occurs in the 
small and medium sized pyramidal cells. Many of the cells 
contain a considerable collection of yellow pigment. There is 
a slight general increase of neuroglia, but no appreciable vascular 
alterations evident by this method of staining. 

Corresponding with the above conditions, sections stained by 
the Marchi iron-alum Pal method show that the fibres composing 
the horizontal systems are decidedly fewer than normal. In 
place of the definite bundles which should occur these fibres are 
few and scattered, the greatest diminution is seen in those 
composing the line of Baillarger and the super- and inter-radial 
groups; the change is not so noticeable in the superficial tan¬ 
gential system. 

Marchi sections do not show any recent degeneration in the 
fibres of the brain; in these sections the intracellular pigment, 
which was yellow by the Nissl or polychrome method, is stained 
black, and the large number of pigmented cells forms a very 
conspicuous feature of the specimens. There is also a very ex¬ 
tensive deposit of black pigment in the endothelial cells of the 

The cerebellum is normal, Purkinje’s cells being numerous, 
well developed, and devoid of pigment. The anterior horn cells 
of the spinal cord are present in normal amount, but many of 
them show signs of slight incomplete development, being small, 
irregular in shape, and with attenuated and rather fewer pro¬ 
cesses than normal. They all contain a considerable collection 
of yellow pigment (Nissl and polychrome). The cells of Clarke's 
column are perfectly normal in every way, and afford a striking 
contrast to those of the anterior horns. In none of the sections 
examined is there any evidence of acute degeneration of either 
cells or fibres. 

Case 2.—(M. T., female, No. in series 81.) Primary amentia; 
simple variety ; medium grade—with epilepsy ; no dementia . 

Family history. —Particulars incomplete. 

Clinical. —The patient is the seventh out of a family of 
eight. She has been dull, backward, and of deficient intellect 



from birth; she did not walk until 5 years of age ; could never 
learn at school; has had epileptic fits since 9 years old. She 
remained at home until 20 years of age, when she became too 
troublesome for her mother to look after and had to be sent 
to the asylum. On admission: she could understand what was 
said to her, and could converse, but in a simple and childish 
manner; she recognised the letters of the alphabet and could 
count a little, but was quite unable to do multiplication or 
division; she was too deficient in intelligence to do any kind 
of work. During the time she was in the asylum there was 
very little change in her condition, she had fairly frequent 
epileptic fits but not of a severe character, and she did not 
become demented. She died at the age of 24 of broncho¬ 
pneumonia with tuberculosis of the small intestine. Numerous 
stigmata of degeneracy were present. Circumference of skull, 
18£ inches. 

Post-mortem appearances .—The skull was symmetrical, but 
very small, dense and thick, there being practically no diploe. 
The dura was slightly thickened; the pia-arachnoid was neither 
thickened nor opaque, and stripped naturally. The vessels and 
sinuses were healthy. The brain was very small, weighing only 
660 grammes (with pons, medulla and cerebellum); the hemi¬ 
spheres were equal and the convolutions of average complexity, 
although very irregular and distorted in their arrangement. 
There was localised agenesis of the upper portions of the occipital 
lobe on both sides, the veins coming from the undeveloped con¬ 
volutions being quite impervious and calcified. The grey 
matter of the cortex was thinner than usual, but there was no 
further naked eye abnormality. 

Microscopical examination .—Sections of the brain were 
examined from the following regions: the first, second, and third 
frontal convolutions, temporo-sphenoidal lobe, the leg and arm 
areas, supramarginal and occipital lobes, the hippocampus, and 
optic thalamus; also from the cerebellum. 

The most noticeable condition present in N issl and poly¬ 
chrome stained sections is an imperfect development of the cells 
of the second and third layers (small and middle sized pyramids). 
These undeveloped cells consist of a large ovoid or pyriform 
nucleus surrounded by a small quantity of finely reticulated 
protoplasm, and without any definite cell processes; the nucleolus 
is frequently eccentric, and therefore in many instances is not 
seen at all Such cells occur in the layer of small pyramids in 
all parts of the brain, but they are undoubtedly more numerous 
in the frontal region, and least so in the central and occipital 



convolutions and in the hippocampus. In the frontal region 
there are, in addition, many neuroblasts exactly like those 
present in the new-born child. Many of the large motor cells 
(Betz) from the top of the ascending frontal convolution are 
also in an imperfectly developed state, they are all shapes and 
sizes, the nucleus is eccentric, they possess but few processes, 
which are attenuated and usually devoid of chromatoplasm; 
the Nissl bodies of the cell are also small and irregular in shape. 
The cells of the hippocampus are certainly better developed 
than those in other regions of the cerebral cortex; the cells of 
the optic thalamus and cerebellum are also well developed and 
offer a striking contrast to those in the other regions examined. 
There is no increase of neuroglia, no vascular change, and no 
sign of acute or chronic degeneration. 

In sections stained by Marchis method it is seen that many 
of the cortical pyramidal cells (both small and large) contain 
a quantity of black granular pigment, this condition being 
especially marked in the cells of the hippocampus. The endo¬ 
thelial cells of nearly all the capillaries contain considerable 
deposits of black pigment. There is an entire absence of acute 
degenerative change in either nerve cells or fibres. 

There is a numerical diminution of all the fibres of the 
horizontal systems, which is most evident in the frontal region 
and least so in the central and occipital. In the undeveloped 
portion of brain from the occipital region there are present 
large numbers of neuroblasts and also of neuroglia cells, many 
of these latter are undergoing division; medullated fibres (both 
projection and association) are present, but their arrangement 
is very irregular and entirely abnormal. 

Case 3.—(M. F., female, No. in series 105.) Primary amentia; 
simple variety; medium grade; with epilepsy and slight 
dementia . 

Family history .—Father died insane aged 59. Father's 
father was a heavy drinker; father's mother lived until 60 years 
of age but had “shaking palsy” for the last forty years; two 
of father's brothers and three of father’s sisters died of phthisis. 
Apparently no injurious influences on the mother's side. The 
patient is the sixth out of a family of. seven; one other is 
hemiplegic from a fit shortly after birth; another became insane 
after influenza but has now recovered, and two died young. 

Clinical .—The patient had convulsions whilst teething, they 



were slight but continued until 8 years of age, since then they 
have become very much worse. She was late in walking and 
talking, and never learned at school, and was never able to 
follow any regular work. Admitted to the asylum, aged 16, as 
she became very violent, troublesome and destructive after fits. 
There was evidence of considerable arrest of mental develop¬ 
ment, the patient being very simple and childish; at the age 
of 21 her intellectual development was no greater than that of 
a child of 4 or 5 years. She was subject to fairly frequent and 
severe epileptic fits, and was at times very violent and aggressive, 
in between the fits appearing to be quite happy playing with 
dolls or children’s toys. A slight amount of dementia gradually 
supervened, and she died at the age of 27 of exhaustion follow¬ 
ing a succession of fits. Typical stigmata of degeneracy were 
present. Circumference of skull, 21^ inches. 

Post-mortem appearances .—The skull was not thickened. 
The dura mater was firmly adherent to the vertex of the skull, 
and there was slight thickening and opacity of the pia along the 
lines of the large fissures; the pacchonian bodies were normal. 
The total weight of the brain was 1,302 grammes, the right and 
left hemisphere being equal. The brain, although of large size, 
was very simply convoluted, no other naked eye change. A 
Meckel’s diverticulum was present. 

Microscopical examination .—Sections of brain were examined 
from the following regions : The first, second and third frontal 
convolutions, the leg area, the temporo-sphenoidal and supra¬ 
marginal lobes, the hippocampus and the occipital lobe. Stained 
b y NissVs method the chief feature of these sections consists 
in a chronic degeneration affecting a very large number of the 
smaller and middle sized pyramidal cells in all parts of the 
brain; this is decidedly most extensive in the frontal lobe and 
m the hippocampus, somewhat less so in the motor region, and 
least marked of all in the occipital lobe. Many of these 
pyramidal cells have almost completely disappeared, being simply 
represented by an irregular collection of debris; in others the 
change is not quite so marked as this, and in some it is but 
slight; there are, however, comparatively few cells which might 
be described as healthy. The large Betz’ cells do not appear to 
be altered. In addition to this atrophic process the cells are 
decidedly irregular and haphazard in their arrangement, but 
individually appear to have been fairly well developed, and 
there is no large number of neuroblasts or imperfectly developed 
cells as in some of the other cases. There is a considerable 



increase in the number of young neuroglia cells in many of 
the sections examined, and here and there the vessels are dis¬ 
tended, and there is alight proliferation of the endothelium of 
the capillaries, but on the whole there is very little vascular 
change to be made out in Nissl sections. In all parts of the 
brain there are more leucocytes than normal, and they are most 
numerous where the degeneration is most marked; in many 
instances two or three leucocytes may be seen in actual contact 
with one of the degenerated nerve cells, which they appear to 
be in process of absorbing. 

In sections stained by Mar chi’s method the majority of the 
pyramidal cells are seen to be almost full of small black granules 
(probably pigment), and this condition is more pronounced in the 
large cells of the hippocampus than in any other region of the 
brain. There is no recent degeneration to be made out in any 
of the fibres. The walls of the capillaries throughout the entire 
brain contain abundant deposits of black pigment, and the same 
condition is observable in the adventitial sheaths of most of the 
middle sized vessels. 

In Mar chi iron-alum Pal sections there is seen to be a pro¬ 
nounced numerical diminution of all the fibres of the horizontal 
systems, all the different layers and all portions of the brain 
appear to be affected to an equal extent. 

Unfortunately it was impossible to make the autopsy in this 
case until forty-eight hours after death, and therefore most of 
the nerve cells show slight evidence of early post-mortem change. 
At the first glance this might possibly be mistaken for an acute 
degeneration, but a most careful examination has convinced me 
that none such is really present; the irregular arrangement of 
the cells and the condition of chronic atrophy associated with 
the deposition of large quantities of pigment cannot, however, 
possibly be mistaken. 

Case 4.— Primary amentia; Mongolian variety . (Age 15 days, 
No. in series 202.) 

(For the central nervous system of this case I am indebted 
to Dr. G. A. Sunderland.) 

The child, a male, presented the characteristic appearances of 
a Mongolian imbecile and died fifteen days after birth. Its 
weight when bom was 4 lbs. 4 ozs.; it had an imperforate anus 
and a stricture of the second part of the duodenum, with dilata¬ 
tion of the first part forming a sac as large as the stomach; 



also the left kidney was cystic and the left ureter dilated; there 
were also signs of congenital syphilis. 

Post-mortem examination. —The brain (with pons, medulla, 
and cerebellum) weighed 340 grammes, being therefore slightly 
smaller than normal; the small size was most observable in the 
cerebellum, which instead of weighing one-thirteenth of the total 
weight was only one-sixteenth. A similar condition of the 
cerebellum has been previously noticed in this variety of idiocy. 
The brain was somewhat simply convoluted, but beyond this 
there was no abnormality apparent to the naked eye, and the 
membranes and vessels were healthy. 

Microscopical examination. Brain. —Differentiation of the 
cells to form the various cortical layers has taken place, but 
many of them are far from being completely developed, especially 
those of the second cortical layer (small pyramids), in this 
situation the majority of the cells being simply neuroblasts; 
around some of these a few irregular strands of protoplasm are 
present, and in a very small number there is an attempt at an 
apical process, but in no case are any other processes present. 

In the next layer (medium pyramids) development is slightly 
more advanced, and the best formed and most completely 
developed of all the cortical cells are seen in the layer of large 
pyramids, but even in this situation some of them retain their 
embryonic features. In all these cells the protoplasm shows a 
great tendency to fall away from the nucleus and to become 
vacuolated. A large number of the neuroblasts and also some 
of the nerve cells are undergoing division, and within many of 
them a very well marked spindle can be seen. There are no 
definite Meynert/s columns, but there are indications of them 
in places. Development is less advanced in the frontal lobes 
than in other portions of the brain; there is no increase of 
neuroglia and no vascular abnormality. 

Cerebellum. —There is a very plentiful and well-defined layer 
of granules lying superficial to the molecular layer (as is usual 
in the embryo and for a short time after birth). The other 
layers appear to be normal, and there are a fair number of 
Purkinje’s cells present, indeed in several places there are small 
nests situated within the granule layer containing a large number 
of these cells. The dentate nucleus is of normal size and con¬ 
tains an abundance of cells. 

Spinal cord. —The length is 150 mm.; the cervical and crural 
enlargements are well marked and there are no naked eye 
abnormalities. The cells of the anterior horns are plentiful and 




well developed, the Nissl bodies being numerous and very large. 
The nerve fibres are not yet myelinated in the crossed and direct 
pyramidal tracts as well as in portions of the antero-lateral and 
posterior columns of the spinal cord; also in parts of the brain, 
mid-brain, and cerebellum. 

Remarks. —Although in this case the development of the 
nerve cells and fibres is of course greatly behind that of the 
adult brain, no appreciable difference can be detected on com¬ 
paring the sections with a normal brain of the same age. 

Case 5.—(W. S., male, No. in series 34.) Primary amentia; 
sclerotic variety; medium grade; with epilepsy and sub¬ 
sequent slight dementia. 

Family history .—Father insane. Father's mother epileptic 
and insane. 

Clinical. —The patient has had fits since 1 year old, and 
has always been of deficient intellect, being unable to learn at 
school and subsequently doing no work. He had to be sent to 
the asylum at the age of 13 as he was too troublesome to be 
managed at home. On admission he was an imbecile of medium 
grade, understanding what was said to him and being able to 
converse, but in a very simple and childish manner; he had 
frequent fits and was subject to occasional paroxysms of excite¬ 
ment, and he was quite unemployed. He gradually passed into 
a state of partial dementia, and died at the age of 19 after 
a succession of 406 epileptic fits. Well-marked stigmata of 
degeneracy were present. 

Post-mortem appearances .—The skull was symmetrical and the 
bone very dense, but not thicker than normal. The dura mater 
and pia-arachnoid membranes were natural, the latter stripping 
with undue readiness from the sclerotic portions of brain 
described below. There was no excess of cerebrospinal fluid. 

Brain. —The weight (including pons and cerebellum) was 
1,445 grammes, representing a considerable increase relative to 
the size of the organ; the two hemispheres were of equal weight. 
On stripping off the pia-arachnoid it was seen that several con¬ 
volutions of both hemispheres were smoother, paler, and had a 
much more compact appearance than the rest of the brain, and 
from these the membrane stripped with great readiness, although 
clinging to the other regions in a natural manner. On making 
a section into these convolutions they were found to be extremely 
firm and dense owing to portions of the brain substance being 



replaced by sclerotic tissue. These sclerotic areas were abundant 
in both hemispheres, being chiefly confined to the superficial 
grey matter, indeed they could not be found in the white matter 
of the centrum ovale; they were frequently irregular in outline, 
although as a rule badly defined and tending to pass gradually 
into the adjacent brain tissue. In the portions involved the 
cortical striae were very irregular and much obscured; but on the 
whole the condition was one more readily appreciable by the 
sense of touch than that of sight, the extreme hardness of the 
areas being their most characteristic quality. 

Attached by a broad base to the corpora striata, and pro¬ 
jecting inwards therefrom into the cavity of the lateral ventricles, 
were numerous small nodules varying in size from that of a 
grape stone to a large pea, and consisting of a very dense tissue 
similar to that in the brain; on section these nodules could 
be seen with the naked eye to slightly infiltrate the adjacent 
portion of the grey matter from which they grew. The lateral 
ventricles were not dilated and the ependyma was normal. 
Cerebellum .—There was obvious naked eye atrophy of several 
leaflets on the upper surface of both hemispheres chiefly con¬ 
fined to the lobus clivi. The medulla and spinal cord showed 
no naked-eye change. 

Microscopical examination .—Sections were examined from 
several regions of the brain, medulla, cerebellum, and spinal cord. 

Brain: The dense areas described above are seen to consist 
largely of glia tissue; in some of them the glia cells are com¬ 
paratively few and of a fully formed appearance, there being 
present an abundant mesh work of fibres; in other areas, however, 
the cells are much more numerous and of more recent forma¬ 
tion, and the sclerosis is not so dense. The areas are not sharply 
defined but pass insensibly into the surrounding brain tissue, 
and they are comparatively poorly supplied with blood vessels. 
The nerve cells of the cortex are very irregularly arranged, their 
apical processes pointing in all directions; in addition a large 
number of them have the ordinary appearance of imperfectly 
developed cells, and a considerable number of actual neuroblasts 
are also present in the superficial layers. A large number of 
the cells, especially the smaller and medium sized pyramids, are 
also undergoing a chronic form of degeneration, being small and 
withered looking, the nuclear membrane often indistinct, the 
processes few and attenuated, and the cell body containing a 
considerable collection of pigment. In the region of the sclerotic 
areas the lamination is very irregular, probably largely the 



result of the neuroglial overgrowth. In some of the convolutions 
there is a dense band of neuroglia on the surface of the brain 
immediately underneath the piararachnoid membrane, and 
superficial to the tangential fibres. The nodules projecting from 
the corpora striata consist of almost pure glia tissue, the cells of 
which have a peculiar whorl-like arrangement; they are covered 
by an ependyma of perfectly normal structure. Sections stained 
by Marchi's method reveal the absence of any recent degenera¬ 
tion amongst the medullated fibres of the white matter. The 
tangential, super- and inter-radial fibres, as well as those com¬ 
posing the outer line of Baillarger, are considerably diminished 
in number in all parts of the brain. There are two or three 
small foci, situated .within the sclerotic areas, in which granules 
of haematoidin occur, apparently indicating an old haemorrhage; 
the endothelial cells of some of the capillaries contain collec¬ 
tions of black pigment (Marchi sections), but otherwise there is 
no structural alteration in the vessels of either the brain or 
membranes, and no evidence of any inflammatory change. 

Cerebellum: Sections of the atrophied portions show that 
there is marked diminution in the number of Purkinje's cells 
and also in the projection fibres ; but Purkinje's cells do not 
contain any pigment like that in the cells of the brain. 

Medulla and cord: There is slight interstitial sclerosis (no 
Marchi change) in the crossed pyramidal tracts traceable as 
far as the mid-dorsal region; also in the antero-laterai columns 
as far down as the fourth cervical segment. The cells df the 
anterior horns are plentiful and well formed, many of them 
contain a considerable collection of pigment which stains 
black with Marchi's stain, but otherwise they appear to be 
normal. There is no sign of any diffuse sclerosis in the cord like 
that met with in the brain. 

Case 6 .— (E. G., female, No. in series 201.) Primary amentia; 
sclerotic variety; low grade. 

Family history.— No friends living and no particulars 

Clinical .—Admitted into the asylum aged 12 years. On ad¬ 
mission: “Very imperfect mental development; she can only 
say a few words and can only understand a very little of what 
is said to her. She is in a condition of general helplessness. 


and spends most of her time sitting in a chair, although there 
does not appear to be any actual paralysis. She is unable to 
do any kind of work or to wash or dress or even feed herself 
without assistance; habits are clean. She is the subject of 
general movements which are choreic in nature, but there are 
no actual convulsions. 1 She remained in the asylum for eight 
years, there being no improvement. According to the notes con¬ 
tractures of the limbs appear to have come on, but the condi¬ 
tion is only casually referred to and there is no account of the 
state of the reflexes, &c. The patient died at the age of 20 
years, of broncho-pneumonia. Numerous stigmata of degeneracy. 
Circumference of skull at the age of 12 years was 19£ inches. 

Post-mortem, appearances. —The skull was small but sym¬ 
metrical, and the membranes and vessels were normal. The brain 
was very small, weighing (with pons and cerebellum) only 896 
grammes. The two hemispheres were of equal size and of fairly 
normal complexity. On making a section of the brain it was 
found to be exceedingly firm and dense, in fact, of almost 
cartilaginous consistence, and the whole of the white matter was 
very much diminished in bulk. The grey matter of the cortex 
was of ordinary thickness but was also very dense. The basal 
. ganglia were firm and fibrous in appearance. The ventricles 
were not dilated and not granular. The cerebellum was also of 
considerably increased consistence, but not so markedly so as the 
brain. The organs of generation were incompletely developed. 

Microscopical examination of the brain shows that on the 
whole there are decidedly fewer nerve cells present than nor¬ 
mally, also that a large number are in a state of incomplete 
development; this is especially marked in the second and third 
layers (small and medium pyramids), where many of the cells 
consist of simply a large nucleus with a few irregular strands 
of protoplasm arranged round it, there being an entire absence 
of processes. Others are somewhat better developed, but ex¬ 
ceedingly irregular in their arrangement, their apical processes 
pointing in all directions. There are also many cells exactly 
resembling the neuroblasts found in the brain of the child at 
birth. Throughout all the sections examined there is a great 
overgrowth of neuroglia both in the grey and white matter, and 
in some regions of the cortex there is quite a definite zone of 
neuroglia lying immediately underneath the piararachnoid mem¬ 
brane ; this increase of neuroglia causing the lamination to 
appear very irregular. In the white matter of the brain, situated 
at a little distance below the cortex, there are found numerous 



scattered islets of a circular shape, within which are many 
incompletely developed nerve cells similar to those occurring in 
the layer of small pyramids, but no medullated fibres; there 
are also numerous neuroglia cells and fibres. These isolated 
portions of ganglionic matter appear to be the result of an 
irregularity in the process of development (heterotopia); the 
nerve cells within them contain granules of black pigment 
(Marchi) although those in other portions of the brain are 
devoid of pigment. 

Marchi sections fail to show any degenerative changes of an 
acute nature in either cells or fibres of the brain or spinal 
cord. The fibres of the horizontal systems are much diminished 
in number, all the layers being affected; the fibres of the pro¬ 
jection system are also fewer than normal. The pia-arachnoid is 
thickened in places; its vessels and also those of the brain are 
distended; the adventitial sheaths of several of the smaller 
arteries contain considerable deposits of black and dark brown 
pigment, but there are otherwise no structural changes in their 
walls, and no indications of haemorrhage. The capillaries are 

Case 7.—(T. C., male, No. in series 1.) Primary amentia; 
simple variety; high grade; subsequently developing 
general paralysis . 

Family history .—Father insane and alcoholic; father's 
mother and all father's brothers and sisters were also alcoholic. 
Phthisis on the mother's side. The patient is the second of a 
family of eight, no miscarriages; the first-born died aged 
months, and the mother was told by the doctor that had it 
lived it would have been blind and an idiot. The fourth child 
in the family has marks of congenital syphilis and is said to be 
very bad tempered. 

Clinical .—The patient was backward in walking and talking, 
and could never learn his lessons at school. At the age of 14 
he began to behave very queerly, he had a “ dreadful temper " 
and would not go to work, and he became very dirty in his 
habits. He was admitted to the asylum, aged 17, in a condi¬ 
tion of mild mania; this gradually passed into dementia, and he 
died at the age of 19 with all the signs of adolescent general 
paralysis. He had several seizures in the fortnight preceding 


Post-mortem appearances .—No marks of syphilis; state of 
nutrition very poor; large bedsores over both buttocks and back 
of sacrum. The appearances of the brain and its membranes 
were characteristic of general paralysis, in addition the brain was 
much more simply convoluted than normally. It weighed (with 
the pons and cerebellum) 1,167 grammes, the left hemisphere 
being 12 grammes lighter than the right. 

Microscopical examination .—Portions of brain were examined 
from the following situations: First and second frontal convolu¬ 
tions, leg and arm areas, Broca's convolution, supramarginal and 
occipital lobes. In all these regions there is a paucity of cells, 
and many of those present are in an imperfectly developed con¬ 
dition, consisting of a large ovoid nucleus with very incomplete 
cell body and processes. Such undeveloped cells are only to be 
found in the second cortical layer (small pyramids), but occur 
in all the regions of the brain examined, although with less 
frequency in the central (motor) and occipital lobes. A large 
number of the pyramidal cells which have attained a somewhat 
more complete development than the above are most irregular 
in their arrangement, their apical processes pointing in all 
directions and some of them being completely upside down. 

In addition to these indications of incomplete development 
there are also many cells undergoing a chronic degeneration; 
these occur in all the layers and all the regions of the brain, 
but to less extent in the occipital lobe than elsewhere. The 
affected cells are small, irregularly shaped, and withered looking, 
their nucleus is eccentric, and their processes are few and broken 
off; they show well-marked chromatolysis and contain a larger or 
smaller amount of pigment, which is yellow in Nissl and poly¬ 
chrome sections, but black in those stained by Marchi's method. 
There is no evidence of acute change in any of the cells and 
practically no increase of neuroglia, the pathological condition 
present being one of imperfect development to which is added 
a chronic degeneration. 

There is a very considerable diminution in the number of 
horizontally coursing fibres in all parts of the brain, on the 
whole it is most marked in the frontal and supramarginal regions 
and least in the occipital; it affects most of all the fibres of 
the super-radial system, next the tangential fibres, and to some¬ 
what less extent those forming the inter-radial group and the 
line of Baillarger. The line of Gennari in the occipital region 
is well developed and appears to be perfectly normal. There is 
some swelling of the pia-arachnoid membrane, and also slight 



cellular proliferation. The vessel walls are a little thickened in 
places, but on the whole there is very little vascular disturbance, 
many of the capillaries appearing to be perfectly normal. The 
endothelial cells do not contain pigment in this case as in several 
of the others. 

Spinal cord .—There is slight interstitial sclerosis with 
diminution in the number of nerve fibres in both direct 
and crossed pyramidal tracts, also in the antero-lateral and 
posterior columns, and in several of the incoming posterior roots. 
Many of the anterior horn cells are undergoing chronic degenera¬ 
tion similar to those of the brain, and they also contain collec¬ 
tions of granular yellow pigment which stains black with Marches 

Case 8.—(L. B., female, No. in series 163.) Primary amentia ; 

simple variety; high grade; subsequently developing 

general paralysis. 

Family history. —Particulars incomplete; mother died of 
general paralysis, aged 42; father is living and said to be in 
good health. 

Clinical. —The patient has had defective eyesight and been 
of deficient intellect from birth. At the age of 15 she under¬ 
went a marked alteration, at times becoming noisy, violent, 
stamping her feet and tearing her clothing, and threatening to 
kill herself; at others being dazed and taking not the slightest 
notice of her surroundings; she gradually became quite regard¬ 
less of personal cleanliness and utterly indifferent to anything 
which happened around her. It was in this condition that she 
was admitted to the asylum at the age of 15 years, and during 
the time she remained there she continued very depressed, silent 
and apathetic, with at times delusions of a persecutory nature 
(that she was followed by dogs, &c.). She finally passed into a 
state of marked dementia and died at the age of 18 with all 
the clinical signs of general paralysis. There were numerous 
stigmata of degeneracy present, as well as marks of congenital 
syphilis. Circumference of skull, 21 f inches. 

Post-mortem appearances .—The skull was symmetrical and of 
normal thickness and density. The dura mater was normal; 
the pia-arachnoid was opaque and considerably thickened in the 
frontal and pre-parietal regions; the pacchionian bodies were 
very prominent, and there was excess of clear cerebrospinal fluid. 
The brain was of fair size, weighing (with the pons and cere- 



bellum) 1,176 grammes; in addition to a somewhat simple 
arrangement of the convolutions the brain presented the charac¬ 
teristic features of general paralysis. 

Microscopical examination .—Sections of the brain were 
examined from the following situations: First frontal, top of 
the ascending frontal and Brocas convolutions, the arm area, 
the parietal, temporo-sphenoidal and occipital lobes. Portions 
of the cerebellum , pons, medulla and spinal cord were also 

In sections of the brain stained by the Nissl and polychrome 
methods there is a marked deficiency in the number of cells, 
also an incomplete development and irregularity in their arrange¬ 
ment; these abnormalities are most evident in the frontal lobes, 
and best marked in the small and middle-sized pyramidal cells. 
In addition a large number of cells throughout all parts of the 
brain are in a state of chronic degeneration; here and there 
the process is somewhat more acute, but on the whole it cannot 
be said that there is a large amount of acute change. There 
is a slight general increase in the amount of neuroglia; the 
vessel walls are somewhat thickened and many of them dis¬ 
tended ; a large number of the capillaries, however, appear to 
be perfectly normal, and their endothelial cells do not contain 
any pigment. The piararachnoid membrane is in a condition 
of chronic thickening, especially in the fore-part of the brain. 
In sections of the leg and arm areas stained by Marclns method, 
there are seen to be a small number of projection fibres, under¬ 
going recent degeneration, but this does not occur in any other 
region. Many of the cells within all the cortical layers contain 
granules of black pigment. 

Sections stained by the Mar chi iron-alum Pal method show 
that there is a considerable diminution in the number of fibres 
of the horizontal systems, e